ATP Cancer Research Results

ATP, Adenosine triphosphate: Click to Expand ⟱
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Adenosine triphosphate (ATP) is the source of energy for use and storage at the cellular level.
Cellular ATP levels are critical for cell survival, and several reports have shown that reductions in cellular ATP levels can lead to apoptosis and other types of cell death in cancer cells, depending on the level of depletion.
Adenosine triphosphate (ATP) is one of the main biochemical components of the tumor microenvironment (TME), where it can promote tumor progression or tumor suppression depending on its concentration and on the specific ecto-nucleotidases and receptors expressed by immune and cancer cells.

Cancer cells, unlike normal cells, derive as much as 60% of their ATP from glycolysis via the “Warburg effect”, and the remaining 40% is derived from mitochondrial oxidative phosphorylation.
Scientific Papers found: Click to Expand⟱
3864- ACNs,    Anthocyanins Potentially Contribute to Defense against Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, ANTs are potent antioxidants that might regulate the free radical-mediated generation of amyloid peptides (Abeta-amyloids) in the brain
*Aβ↓,
*ROS↓,
*cognitive↑, Mulberries are a rich source of ANTs that induce antioxidant enzymes and promote cognition
*APP↓, In the cerebral cortex, blackcurrant and bilberry extract reduced APP levels in AD mouse models, but changes in the expression or phosphorylation of tau-protein were not observed
*BBB↑, ANTs cross the blood-brain barrier and protect brain tissue from Abeta toxicity
*Ca+2↓, Aronia melanocarpa. ANTs of this plant decrease intracellular calcium and ROS but increase ATP and mitochondrial potential.
*ATP↑,
*BACE/β-secretase↓, An-NPs also attenuate the protein expression of BACE-1 neuroinflammatory markers, such as phosphonuclear factor kB (p-NF-kB), tumor-necrosis factor (TNF-α), and inducible nitric oxide synthase (iNOS),
*p‑NF-kB↓,
*TNF-α↓,
*iNOS↓,

3447- ALA,    Redox Active α-Lipoic Acid Differentially Improves Mitochondrial Dysfunction in a Cellular Model of Alzheimer and Its Control Cells
- in-vitro, AD, SH-SY5Y
*ATP↑, Incubation with ALA showed a significant increase in ATP levels in both SH-SY5Y-APP695 and SH-SY5Y-MOCK cells.
*MMP↑, MMP levels were elevated in SH-SY5Y-MOCK cells, treatment with rotenone showed a reduction in MMP, which could be partly alleviated after incubation with ALA in SH-SY5Y-MOCK cells.
*ROS↓, ROS levels were significantly lower in both cell lines treated with ALA.
*GlucoseCon↑, benefits to diabetic neuropathy and impaired glucose uptake, and the regeneration of glutathione (GSH) and vitamins C and E
*GSH↑,
*neuroP↑, ALA seems to have a positive effect on neurodegenerative diseases such as AD
*cognitive↑, ALA improves cognitive performance and could be considered as a promising bioactive substance for AD by affecting multiple mechanisms such as:
*Ach↑, (1) impaired acetylcholine production;
*Inflam↓, (2) hydroxyl radical formation, ROS production, and neuroinflammation;
*Aβ↓, (3) impaired amyloid plaque formation;
OXPHOS↓, ALA has also been shown to restore the expression of OXPHOS complexes in HepG2 cells, ranging in a concentration between 0.5–2 mM

3545- ALA,    Potential therapeutic effects of alpha lipoic acid in memory disorders
- Review, AD, NA
*neuroP↑, potential therapeutic effects for the prevention or treatment of neurodegenerative disease
*Inflam↓, ALA is able to regulate inflammatory cell infiltration into the central nervous system and to down-regulate VCAM-1 and human monocyte adhesion to epithelial cells
*VCAM-1↓, down-regulate vascular cell adhesion molecule-1 (VCAM-1) and the human monocyte adhesion to epithelial cells
*5HT↑, ALA is able to improve the function of the dopamine, serotonin and norepinephrine neurotransmitters
*memory↑, scientific evidence shows that ALA possesses the ability to improve memory capacity in a number of experimental neurodegenerative disease models and in age-related cognitive decline in rodents
*BioAv↝, Between 27 and 34% of the oral intake is available for tissue absorption; the liver is one of the main clearance organs on account of its high absorption and storage capacity
*Half-Life↓, The plasma half-life of ALA is approximately 30 minutes. Peak urinary excretion occurs 3-6 hours after intake.
*NF-kB↓, As an inhibitor of NF-κβ, ALA has been studied in cytokine-mediated inflammation
*antiOx↑, In addition to the direct antioxidant properties of ALA, some studies have shown that both ALA and DHLA and a great capacity to chelate redox-active metals, such as copper, free iron, zinc and magnesium, albeit in different ways (
*IronCh↑, ALA is able to chelate transition metal ions and, therefore, modulate the iron- and copper-mediated oxidative stress in Alzheimer’s plaques
*ROS↓, iron and copper chelation with DHLA may explain the low level of free radical damage in the brain and the improvement in the pathobiology of Alzheimer’s Disease
*ATP↑, ALA may increase the mitochondrial synthesis of ATP in the brain of elderly rats, thereby increasing the activity of the mitochondrial enzymes
*ChAT↑, ALA may also play a role in the activation of the choline acetyltransferase enzyme (ChAT), which is essential in the anabolism of acetylcholine
*Ach↑,
*cognitive↑, One experimental study has shown that in rats that had been administered ALA there was an inversion in the cognitive dysfunction with an increase in ChAT activity in the hippocampus
*lipid-P↓, administration of ALA reduces lipid peroxidation in different areas of the brain and increases the activity of antioxidants such as ascorbate (vitamin C), α-tocopherol (vitamin E), glutathione,
*VitC↑,
*VitE↑,
*GSH↑,
*SOD↑, and also the activity of superoxide dismutase, catalase, glutathione-peroxidase, glutathione-reductase, glucose-6-P-dehydrogenase
*Catalase↑,
*GPx↑,
*Aβ↓, Both ALA and DHLA have been seen to inhibit the formation of Aβ fibrils

5326- ALC,    L-Carnitine Is an Endogenous HDAC Inhibitor Selectively Inhibiting Cancer Cell Growth In Vivo and In Vitro
- vitro+vivo, Liver, HepG2
TumCG↓, Here we found that (1) LC treatment selectively inhibited cancer cell growth in vivo and in vitro;
P21↑, (2) LC treatment selectively induces the expression of p21cip1 gene, mRNA and protein in cancer cells
ac‑H3↑, (4) LC increases histone acetylation and induces accumulation of acetylated histones both in normal thymocytes and cancer cells
HDAC↓, (5) LC directly inhibits HDAC I/II activities via binding to the active sites of HDAC and induces histone acetylation and lysine-acetylation accumulation in vitro;
*ATP↑, LC is able to generate ATP in normal mouse thymocytes, but not in hepatic HepG2 and SMMC-7721 cancer cells.
selectivity↑,
ac‑H4↑, LC dose-dependently increased acetylation of H3 and H4 (

3159- Ash,    Neuroprotective effects of Withania somnifera in the SH-SY5Y Parkinson cell model
- in-vitro, Park, SH-SY5Y
*neuroP↑, Neuroprotective effects of Withania somnifera
*Inflam↓, including inflammation and oxidative stress reduction, memory and cognitive function improvement.
*ROS↓,
*cognitive↑,
*memory↑,
*GPx↑, significantly increased glutathione peroxidase activity
*Prx↓, KSM-66, had peroxiredoxin-1 and VGF levels significantly lower than the untreated control
*ATP↑, rescue of mitochondria with 0.5 mg/ml KSM-66 extract showed an increase in ATP levels.
*Vim↓, Pre-treatment with KSM-66 decreased level of vimentin
*mtDam↓, KSM-66 attenuates 6-OHDA-induced mitochondrial dysfunction in SH-SY5Y cells

6542- BSB,    Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol
- Review, Var, NA - Review, Park, NA - Review, AD, NA
AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2/PTGS2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE/β-secretase↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2/PTGS2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2/PTGS2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,

2348- CAP,    Recent advances in analysis of capsaicin and its effects on metabolic pathways by mass spectrometry
- Analysis, Nor, NA
Warburg↓, Capsaicin inhibits the Warburg effect by binding directly to Cys424 residue and LDHA of pyruvate kinase isoenzyme type M2 (PKM2).
*PKM2↓,
*COX2/PTGS2↓, capsaicin targets COX-2 and down-regulates its expression, which results in the further inhibition of inflammation
*Inflam↓,
*Sepsis↓, capsaicin may be used as a new active ingredient to treat sepsis and inflammation
*AMPK↑, capsaicin activates adenylate-activated protein kinase (AMPK) and protein kinase A (PKA), in turn enhancing the activity of the mitochondrial respiratory chain and promoting fatty acid oxidation
*PKA↑,
*mitResp↑,
*FAO↑,
*FASN↓, capsaicin can inhibit the activity of fatty acid synthetase
*PGM1?,
*ATP↑, treatment resulted in increased intracellular ATP levels (the end product of glycolysis)
*ROS↓, Capsaicin can mitigate the negative effects of oxidative stress on human health by scavenging these free radicals and reducing the oxidative stress response.

5926- CAR,    An Updated Review of Research into Carvacrol and Its Biological Activities
- Review, Nor, NA - Review, AD, NA - Review, Asthma, NA
*Inflam↓, ic, analgesic, anti-inflammatory,antioxidant, and neuroprotective effects.
*antiOx↑,
*neuroP↑, Carvacrol has exhibited notable neuroprotective effects in experimental models of cognitiveimpairment and neurodegenerative diseases
*BioAv↑, advances in encapsulation andnanotechnology have enhanced its stability and bioavailability
*toxicity↓, Compared to phenol, carvacrol and thymol exhibitsignificantly lower toxicity. This makes carvacrol a safer alternative for various applications, frombiological agents to dietary supplements [
*Pain↓, Pain-Relieving Mechanisms of Car
*TRPV3↑, , carvacrol-induced TRPV3 activation enhances lipolysis in adipocytes via theNRF2/FSP1 a
*NRF2↑,
*Ca+2↑, TRPV3 activation in distal colon epithelial cells elevates intracellular Ca²⁺ levels and stimulates ATP release, implicating carvacrol in gut physiology and signaling
*ATP↑,
*5LO↓, s, including the inhibition of angiotensin-converting enzyme 2 (ACE2), lipoxygenase(LOX), and cyclooxygenase (COX) enzyme
*COX2/PTGS2↓,
PGE2↓, arvacrol’s anti-inflammatory effects involve theinhibition of prostaglandin E₂ (PGE₂) production via COX-2
*hepatoP↑, Carvacrol in Hepatic Protection as Natural Antioxidant
*AntiAg↑, Carvacrol has demonstrated significant antiplatelet activity, highlighting its potential therapeutic role in preventing thrombosis
*Diar↓, s essentialoil exhibited antidiarrheal effects in castor oil-induced diarrhea models, potentially mediated bymechanisms involving Kv channel activation and Ca²⁺ channel inhibition
*cardioP↑, em as promising nutraceutical candidates for alleviatingCVD-related complicat
*other↝, Carvacrol was evaluated for its therapeutic potential in managing erectile dysfunction (ED)associated with aging
*chemoPv↑, Chemopreventive Potential of Carvacrol in Detoxification pathways
*cognitive↑, carvacrol(0.5–2 mg/kg) and thymol significantly improved cognitive function in rats
*AChE↓, potent acetylcholinesterase inhibitory activity (IC₅₀: 158.94 μg/mL)
*GastroP↑, . Gastroprotective Effects of Carvacrol and Mechanism
*eff↑, . When combined with polysorbate 80 as a surfactant, carvacrol was efficiently deliveredto embryonic tissues, maintaining bioavailability during the peri-hatching phase
*BChE↓, acrol. The essential oil rich in carvacrol showedstrong inhibitory effects on AChE and butyrylcholinesterase (BChE) [
*CRP↓, d Phase II clinical trial, asthmatic patients whoreceived 1.2 mg/kg/day of carvacrol for two months showed significant improvements in pulmonaryfunction tests and a notable reduction in C-reactive protein levek

6650- Cen,    Therapeutic Potential of Centella asiatica and Its Triterpenes: A Review
- Review, AD, NA
*BioAv↝, madecassoside, asiaticoside, madecassic acid, and asiatic acid are widely distributed in the body and madecassoside, asiaticoside may exert their biological activity through converted into aglycone (madecassic acid, and asiatic acid).
*BioAv↝, C. asiatica enhances the function of the nervous system. It dissolves in methanol, ethanol, and water.
*MDA↓, Male Wistar rats – MDA ↓, GSH ↑, SOD ↑, AChE↓
*GSH↑,
*SOD↑,
*AChE↓,
*memory↑, Male SD rats; hippocampal cell – Spatial working memory↑, Ki-67 cells↑
*Ki-67↑,
*Catalase↑, Male SD rats MAPK SOD↑, LPO↑, CAT↑, GSH↑, dopamine↑, glutamate↑, Syn1↑, Stx1A↑, PI3K↑, PDK1↑, PEBP↓, VMAT2↑, TH ↑, MAPK ↑, BDNF↑, NGF↑
*PI3K↑,
*BDNF↑,
*NGF↑,
*ROS↓, Water extract of CA Tg2576 mice – ROS↓, NRF2↑, GCLC↑, HMOX1↑, NQO1↑, ATP↑, Mt-ND1↑, Mt-ATP6↑, Mt-CO1↑, Mt-CYB↑, oxygen consumption rate↑
*NRF2↑,
*HO-1↑,
*NQO1↑,
*ATP↑,
*OCR↑,
*TNF-α↓, Ethanolic extract of CA Male SD rats – TNF-α↓, BDNF↑
*PP2A↑, Ethanolic extract of CA Male albino Wistar rats PP2A/GSK-3B PP2A↑, GSK-3B↓, Bcl-2↑
*GSK‐3β↓,
*Bcl-2↑,
*TrkB↑, Standardized extract of CA Male Wistar rats – NR2A↑, NR2B↑, BDNF↑,TrkB↑
*NOTCH1↑, Asiatic acid Male SD rats – Notch1↑, SOX2↑, DCX↑, Nrf2↑, nestin↑, p21 positive cells↓, MDA↓
*SOX2↑,
*Nestin↑,
*MDA↓,
*MAOA↓, Asiaticoside-D Worms – MAO-A↓, MAO-B↓
*MAOB↓,
*GPx↑, Previous studies found that C. asiatica and its triterpenoids could effectively increase SOD and GPX activities, activate nuclear factor erythroid-2-related factor 2, improve the cognitive impairment of animals,
*cognitive↑,
*ROS↓, C. asiatica and its triterpenoids could reduce ROS production
*neuroP↑, they reduced related nerve cell apoptosis, increased synaptic density, and improved the survival rate of neural cells
*glucose↓, Methanol extract of CA Male SD rats – Blood glucose ↓, food and water intake ↓, ALT↓, AST↓, PFK ↑, GS ↑, GP↑, glycogen content ↑
*ALAT↓,
*AST↓,
*PFK↓,
*Weight↓, inhibit weight gain
*Inflam↓, (4) ameliorate inflammation,
*AntiDiabetic↑, C. asiatica extract and related components (asiatic acid, madecassoside) for the treatment of endocrine diseases such as diabetes, obesity and osteoporosis are excellent.
*Obesity↓,
*Wound Healing↑, The C. asiatica extract and its triterpenoids had certain therapeutic and relieving effects on acne, baldness, vitiligo, atopic dermatitis, and wounds. C. asiatica extract can effectively promote wound healing in diabetic patients
*cardioP↑, C. asiatica has a positive effect on cardiovascular diseases.
*GutMicro↑, C. asiatica and its triterpenoids also have therapeutic effects on digestive disorders, which is mainly reflected by improved liver fibrosis, colitis, and gastric mucosal damage; and even reduced Helicobacter pylori gastric colonization
*Sepsis↓, Asiatic acid can improve the side effects caused by antibiotics, reverse multidrug resistance (MDR), and reduce sepsis.
*BioAv↑, C. asiatica cream containing 5.12% asiaticoside and 5.1% madecassoside can be completely absorbed by the skin and effectively improve pigmentation and may be used in treating hypertrophic scars

6632- Cic,    Chicoric Acid Ameliorates Lipopolysaccharide-Induced Oxidative Stress via Promoting the Keap1/Nrf2 Transcriptional Signaling Pathway in BV-2 Microglial Cells and Mouse Brain
- vitro+vivo, Nor, NA
*antiOx↑, chicoric acid (CA) has been well-documented due to its excellent antioxidant and antiobesity bioactivities.
*Obesity↓,
*NRF2↑, CA could insert into the pocket of Keap1 and up-regulated Nrf2 signaling and, thus, transcriptionally regulate downstream expressions of antioxidant enzymes including HO-1 and NQO-1
*HO-1↑,
*NQO1↑, 80 μM CA resulted in noticeably increasing in the levels of the expressions of HO-1 and NQO-1
*ROS↓, CA reduced LPS-stimulated ROS over-release
*GSH↑, CA directly quenched free radicals or by increased antioxidant enzymes such as GSH, CAT and SOD
*Catalase↑,
*SOD↑,
*ATP↑, Moreover, CA alleviated the reduction of energy molecule ATP
*COX2/PTGS2↓, Previous of our research proved that CA promoted glucosamine-mediated glucose uptake and ihibited the expressions of COX-2 and iNOS
*iNOS↓,
*neuroP↑, CA could be considered a promising nutritional complement in oxidative stress-related neuroinflammation.

1577- Citrate,    Citric acid promotes SPARC release in pancreatic cancer cells and inhibits the progression of pancreatic tumors in mice on a high-fat diet
- in-vivo, PC, NA - in-vitro, PC, PANC1 - in-vitro, PC, PATU-8988 - in-vitro, PC, MIA PaCa-2
Apoptosis↑, citrate treatment demonstrates signifcant effcacy in promoting tumor cell apoptosis, suppressing cell proliferation, and inhibiting tumor growth in vivo
TumCP↓,
TumCG↑,
SPARC↑, citrate treatment reveal decreased glycolysis and oxygen consumption in tumor cells, increased SPARC protein expression, and the promotion of M1 polarization
Glycolysis↓,
OCR↓,
pol-M1↑, repolarizing M2 macrophages into M1 macrophages
pol-M2 MC↓, shift from the M2 phenotype to the M1 phenotype in TAMs following citrate treatment
Weight∅, no signficant changes in body weight observed between the two groups
ATP↓, decreased ATP production of pancreatic tumors in vivo
ECAR↓, signifcantly reduced glycolytic flux, glycolytic reserve, glycolytic capacity, and acidifcation rates
mitResp↓, decreased basal mitochondrial respiration
i-ATP↑, decrease in intracellular ATP levels
p65↓, citrate effectively suppressed the expression of RELA findings collectively underscore the critical role of RELA in mediating citrate's regulation of glycolysis and suppression of pancreatic cancer progression
i-Ca+2↑, inhibition of RELA resulted in a rapid elevation of intracellular calcium levels
eff↓, overexpression of RELA and SPARC knockdown attenuated the therapeutic effects of citrate

6298- Cro,    Crocetin Prevents RPE Cells from Oxidative Stress through Protection of Cellular Metabolic Function and Activation of ERK1/2
- in-vitro, AMD, RPE-1
*ATP↑, crocetin pre-treatment protects ARPE19 cells from TBHP-induced LDH release, intracellular ATP depletion, nuclear condensation, and disturbance of junctional integrity and cytoskeleton.
*antiOx↑, a natural antioxidant, such as crocetin, represents a promising candidate to prevent oxidative stress in RPE cells and might halt or delay disease progression in AMD.
*ROS↓,

6293- Cro,    Crocetin: an agent derived from saffron for prevention and therapy for cancer
- Review, Var, NA
*toxicity↓, It has been demonstrated that oral administration of saffron extract at doses from 0.1 to 5 g/kg was non-toxic in mice
*lipid-P↓, crocetin showed significant effects on coronary heart disease by inhibiting lipoprotein oxidation
*neuroP↑, on neurodegenerative diseases [33, 39-44], on retinal function recovery by increasing retinal blood flow [33, 45], on reducing blood pressure and maintaining kidney function
*BloodF↑,
*BP↓,
*RenoP↑,
*ATP↑, enhance oxygen diffusivity during shock and reperfusion that ultimately lead to increased ATP production
AntiCan↑, Saffron and its derivatives particularly crocetin have demonstrated significant anticancer activity in breast, lung, pancreatic and leukemic cells.
TumCP↓, Breast Cancer MCF-7, MDA-MB-231 ↓Proliferation
Apoptosis↑, ↑Apoptosis
lipid-P↓, Liver Cancer Wistar rat (AFB1) C3H1OT1/2 cells ↓Lipid perxidation
ROS↓, Liver Cancer Wistar rat (AFB1) C3H1OT1/2 cells ↓Reactive oxygen species
GSTs↑, Lung Cancer Swiss albino mice (B[a]P) ↓ Lipid peroxidation, ↑GST, ↑catalases, ↑superoxide dismutase
Catalase↑,
SOD↑,

2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2/PTGS2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency

6408- CUR,    Protective Effects of a Natural Product, Curcumin, against Amyloid β Induced Mitochondrial and Synaptic Toxicities in Alzheimer'S Disease
- in-vitro, AD, SH-SY5Y
*mtDam↓, Mitochondrial function and cell viability were elevated in curcumin treated cells.
*eff↓,
*eff↑, Further, the protective effects of curcumin were stronger in pretreated SHSY5Y cells than in post-treated cells, indicating that curcumin works better in prevention than treatment in AD-like neurons.
*FIS1↓, significantly increased in Drp1, by 2.0 fold (p=0.004), and in Fis1, by 2.1 fold (
*lipid-P↓, lipid peroxidation were found ( p=0.002) in Aβ treated relative to untreated cells (figure 4). However, sig- nificantly decreased levels were found in the curcumin treated cells ( p=0.02) relative to untreated cells.
*ATP↑, Significantly increased levels of ATP were found in cells treated with curcumin

1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.

7235- EGb 761,    Stabilization of Mitochondrial Membrane Potential and Improvement of Neuronal Energy Metabolism by Ginkgo Biloba Extract EGb 761
- in-vitro, AD, NA
*MMP↑, EGb 761 given shortly after initiating mitochondrial damage by sodium nitroprusside (nitric oxide donor) improved the mitochondrial membrane potential of PC12 cells significantly and dose dependently.
*ATP↑, EGb 761 also reversed the decrease in ATP production. In addition, similar protection against oxidative damage was found in dissociated brain cells and isolated brain mitochondria after in vitro or in vivo treatment with EGb 761.

7240- EGb 761,    EGb 761 protects liver mitochondria against injury induced by in vitro anoxia/reoxygenation
- in-vitro, Nor, NA
*ATP↑, In conclusion, EGb 761 specially protects mitochondrial ATP synthesis against anoxia/reoxygenation injury by scavenging the superoxide anion generated by mitochondria.
*ROS↓,
*hepatoP↑, EGb 761 protects liver mitochondria against injury induced by in vitro anoxia/reoxygenation

6829- EMD,    Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug
*diuretic↑, diuretic, vasorelaxant, anti-bacterial, anti-viral, anti-ulcerogenic, anti-inflammatory, and anti-cancer effects.
*Bacteria↓,
*AntiViral↑,
*Inflam↓,
AntiCan↑,
*cardioP↑, timely overview of emodin related to the treatment of cardiovascular disease.
*NF-kB↓, graphic abstract Immunomoduation
*TNF-α↓,
*IL1β↓,
*NO↑,
*eNOS↑,
*PPARγ↑,
*Casp9↓, anti-apoptosis
*Casp3↓,
*GSDMD↓,
*Bcl-2↑,
*STAT3↑,
*ATP↑, anti-oxidant
*SOD↑,
*GSH↑,
*HDAC2↓, anti cardiac hypertrophy
*SIRT3↑,
ROS↑, anti-proliferative
PCNA↓,
P53↑,
cMyc↓,

4251- FA,    Antidepressant-Like Effect of Ferulic Acid via Promotion of Energy Metabolism Activity
- in-vivo, NA, NA
*BDNF↑, FA increases catecholamine (dopamine and noradrenaline), brain-derived neurotrophic factor, and ATP levels, and decreases glycogen levels in the limbic system of the mice brain.
*ATP↑,
*Mood↑, antidepressant-like effects of FA observed in this study

6981- Form,    Formononetin: a review of its source, pharmacology, drug combination, toxicity, derivatives, and drug delivery systems
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
BioAv↝, FMN has only one phenolic hydroxyl group, so it is poorly soluble in water and easily soluble in organic solvents such as methanol, ethyl acetate, and ether.
*memory↑, It had been found that FMN, isolated from Sophora secundiflora, could improve memory problems by restoring the level of oxidative stress in brain tissues and modulating acetylcholinesterase activity. I
*ROS↓, findings suggest that FMN can inhibit oxidative stress in the liver and restore mitochondrial function
*AChE↓,
*NF-kB↓, FMN, the expression levels of the above three decreased and NF-κB activation was inhibited, which may be related to the release of FMN blocking kelch-like ECH-associated protein-1 (Keap1) and activating the nuclear factor erythroid 2-related factor 2
*Keap1↝,
*NRF2↑,
*Inflam↓, FMN exerted anti-neuroinflammatory effects by targeting peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) and bidirectionally regulating NF-κB signaling pathway and Nrf2/Heme oxygenase-1 (HO-1) signaling pathway,
*PGC-1α↝,
*HO-1↓,
*p‑tau↓, thereby inhibiting tau protein hyperphosphorylation.
*cognitive↑, Significantly FMN improve cognitive dysfunction in mice caused by high-fat feeding
*BDNF↑, increased BDNF and 5-hydroxytryptamine (5-HT) levels, and mitigated the progression of depression in mice.
*5HT↑,
*Stroke↓, It could significantly reduce the level of inflammatory factors, increase the number of dendritic spines in neurons, and increase the expression of βIII-tubulin, growth-associated protein 43 (GAP-43), nerve growth factor (NGF) and BDNF.
*PARP1↓, FMN significantly reduced PARP1, PARG, apoptosis-inducing factor (AIF), cysteinyl aspartate-specific protease 3 (caspase-3) and p53 protein in rats with cerebral ischemia-reperfusion injury
*AIF↓,
*Casp3↓,
NP/CIPN↓, FMN had a favorable ameliorative effect on oxaliplatin-induced peripheral neuropathy and did not affect the chemotherapeutic function of oxaliplatin.
*neuroP↑, The neuroprotective mechanism of FMN is shown in Figure 2.
*NGF↑,
*TNF-α↓,
*IL1β↓,
*IL18↓,
*IL6↓,
*VCAM-1↓,
*pol-M2 MC↑,
*hepatoP↑, could reduce hepatotoxicity and improve liver function through inflammatory molecular pathways.
*AST↓, reduce serum AST, ALT, TNF-α and IL-1β levels. I
*ALAT↓,
*LC3II↑, the levels of LC3II, Beclin1, p62, cyclooxygenase-2 (COX2), COX4, MMP and adenosine triphosphate (ATP) were increased
*Beclin-1↑,
*p62↑,
*COX2/PTGS2↑,
*MMP↑,
*ATP↑,
*GSH↑, activity of antioxidant proteins glutathione (GSH), catalase (CAT), GSH-PX in the FMN treatment group recovered, and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) decreased.
*Catalase↑,
*GPx↑,
*MDA↓,
*antiPs↑, it was found that the interferon (IFN) signaling pathway was inhibited, which could effectively reduce the expression of related inflammatory chemokines, and significantly improve the erythema, scales and thickness of skin lesions in the psoriasis m
*AntiDiabetic↑, FMN effectively mitigated alloxan-induced pancreatic β-cell and DNA damage, lowered blood glucose levels, and increased insulin content.
*glucose↓,
*Insulin↑,
*GutMicro↑, FMN could act as a prebiotic to regulate intestinal microbial flora, thereby improving host metabolism and preventing obesity
*Obesity↓,
COX2/PTGS2↓, FMN effectively inhibited the proliferation of KYSE170 and KYSE150 cells by significantly reducing the mRNA and protein expression levels of COX-2 and cyclin D1, while inducing G1 phase arrest.
cycD1/CCND1↓,
TumCCA↑,
EGFR↓, FMN binds to both WT and mutant EGFR, reducing EGFR kinase activity and inhibiting downstream signaling.
GSK‐3β↑, This, in turn, activated GSK-3β and decreased the expression of myeloid leukemia sequence 1 (Mcl-1), without causing significant toxicity to the vital organs of mice.
Mcl-1↓,
*toxicity↓,
TumCP↓, FMN inhibited the proliferation and growth of cervical cancer cells by inhibiting the expression of HIF-1-α and VEGF.
Hif1a↓,
VEGF↓,
ERK↓, can achieve antiproliferative and invasive effects through effective inhibition of the oncogenic ERK1/2 pathway and the Lamin A/C signaling pathway,
LAMs↓,
Cyt‑c↑, FMN, as a candidate anticancer drug, could release cytochrome C (cyto C) directly through the mitochondrial pathway and activate the cascade reaction of caspase-9, caspase-3 and PARP, which ultimately lead to FaDu cell death
Casp9↑,
Casp3↑,
PARP↑,
TumCD↑,
mitA↑, FMN inhibited mitosis by inactivating the BACH1/p53 signaling pathway, promoted the release of cyto C
BACH1↓,
P53↓,
ROS↑, FMN delivered ROS to mitochondria to release cyto C and activated caspase-3 and caspase-9 cascade reactions to induce apoptosis in MCF7 cells
PD-1↓, FMN has the potential to serve as a PD-1/PD-L1 inhibitor for clinical use
NF-kB↓, FMN mainly interfered with PD-L1 activation by inhibiting the STING-NF-κB signaling pathway
*Bacteria↓, possess other pharmacological activities, such as antibacterial, antiviral, and antiallergic
*AntiViral↑,
*mt-ROS?, FMN effectively reduced the accumulation of ROS and mitochondrial damage in hair cells by activating the PI3K/AKT-Nrf2 signaling pathway, restored the balance of GSH/GSSG.
*PI3K↓,
*chemoP↑, FMN was a potential therapeutic agent for cisplatin-induced ototoxicity.
ChemoSen↑, Therefore, combination therapy had better control effects on multiple targets and a lower risk of drug resistance, which had great application prospects for treating cancer.
eff↑, combination of FMN (30 μM) and sulforaphane (20 μM) exhibited a significant synergistic effect
*toxicity↓, Therefore, it was proved that FMN was safe and non-toxic and could be used for pharmacological and therapeutic purposes.
*BioAv↑, water solubility problem of FMN, succinylated FMN using Bacillus amyloliquefaciens FJ18 to form the compound FMN-7-O-β-D (6″-O-succinyl)-D-glucoside (FMP), which compared to FMN, the water solubility was increased more than 106-fold.
*BioAv↑, To solve those problems, structural modification and nano-delivery systems can be used as a promising solution
*eff↑, FMN can be combined with other treatments, such as immunotherapy, to enhance the therapeutic effect and improve the prognosis of patients;

7195- GBE,    Mitochondrial effects of Ginkgo biloba extract
- Review, AD, NA
*ROS↓, A growing volume of data confirms that Ginkgo biloba extract (GBE) reduces oxidative stress and improves mitochondrial respiration and thus may be useful in preventing or slowing down the progression of AD.
*mitResp↑,
*AntiAge↑, Treatment of Caenorhabditis elegans with GBE- extract reduces oxidative stress and extends median lifespan compared with controls.
*ATP↑, In older mice, GBE resulted in a protective effect by increasing production of adenosine triphosphate in neurons
*neuroP↑, The flavonoids, bilobalide and some of the ginkgolides (B and J) had a high protective capacity
*ETC↑, (ETS) were also examined, with interesting results. Complex I activity was significantly increased after APP cells but not control cells were treated with Ginkgo biloba extrac
*compI↑,

7212- GBE,    The Use of Ginkgo Biloba L. as a Neuroprotective Agent in the Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, The antioxidant effects of EGb 761 are mainly related to its influence on cerebral blood flow, the neurotransmitter system, cellular redox state and the level of nitric oxide
*ROS↓, EGb 761 works directly by scavenging ROS or increasing the expression of genes encoding antioxidant enzymes
*mitResp↑, When used, it reduces oxidative stress, improving mitochondrial respiration (Müller et al., 2019) and protects cells from NO-induced neurotoxicity by reducing the increase in caspase-9 activity that activates caspase-3, leading to cell apoptosis
*Casp9↓,
*Casp3↓,
*Apoptosis↓,
*ATP↑, EGb 761 reduces the production of ROS in the mitochondria and protects the mitochondrial complexes of the respiratory chain and increases the availability of ATP
*neuroP↑, Neuroprotective Effect of G. biloba
*IL1β↓, IL-1β, IL-6 and TNFα, causing pro-inflammatory reactions, however, anti-inflammatory cytokines such as IL-4, IL-13 and Arg-1 are also secreted in microglia activation. The use of EGb 761 significantly reduces the above-mentioned cytotoxic mediators,
*IL6↓,
*TNF-α↓,
*PGE2↓, EGb 761 extract strongly inhibits LPS-induced prostaglandin E2 (PGE 2) production mediated by cyclooxygenase 2 (COX-2)
*memory↑, The main reasons for the improvement in memory and cognitive functions after the use of G. biloba include: increased blood flow in the brain, protective effect against peroxidation of brain lipids, easier utilization of oxygen and glucose by brain ce
*cognitive↑,
*BloodF↑,
*lipid-P↓,
*Aβ↓, reduction of amyloid plaque deposition
*MAOA↓, EGb 761 can effectively reduce the activity of MAO, as well as increasing the level of dopamine, especially in the prefrontal cortex
*DA↑,
*Dose↝, In general, the EGb 761 extract is well tolerated and safe up to a dose of 240 mg/day
*toxicity↓, The oral LD50 in mice is 2,100 times the recommended daily dose

7482- H2,    Molecular Hydrogen Therapy: Mechanisms, Delivery Methods, Preventive, and Therapeutic Application
- Review, Var, NA - Review, IBD, NA - Review, Stroke, NA - Review, Sepsis, NA - Review, AD, NA
Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.

7483- H2,  Cisplatin,    Molecular hydrogen attenuates cisplatin-induced nephrotoxicity by modulating β-hydroxybutyrate metabolism
- in-vivo, Nor, HK-2
RenoP↑, H2 inhalation significantly attenuated cisplatin-induced kidney injury by reducing inflammation and apoptosis in renal tissue.
BHB↑, H2 upregulated the ketone body metabolic pathway, particularly enhancing β-hydroxybutyrate (β-HOB) synthesis via increased expression of the ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2).
HMGCS2↑,
chemoP↑, Molecular hydrogen confers protection against cisplatin-induced nephrotoxicity by modulating β-HOB metabolism through upregulation of HMGCS2, thereby suppressing renal inflammation and apoptosis.
*IL2↓, IL-1β, IL-6, MCP-1, and TNF-α in kidney tissue. Levels of these proinflammatory mediators were significantly elevated following cisplatin treatment. H2 inhalation significantly suppressed these cytokines,
*IL6↓,
*MCP1/CCL2↓,
*TNF-α↓,
*KeyT↝, H2 upregulated HMGCS2 to enhance ketone body metabolism
*Inflam↓, H2 has been demonstrated protective effects in various inflammatory and oxidative stress-related conditions
*ROS↓,
*MMP↑, Several studies have shown that H2 can preserve mitochondrial membrane potential, boost ATP generation, and improve mitochondrial dynamics and biogenesis by activating pathways such as mitofusin-2 (Mfn2) and PGC-1α
*ATP↑,
*MFN2↑,
*PGC-1α↑,
*BUN↓, Our work confirmed that H2 inhalation significantly ameliorated cisplatin-induced histological damage, elevated BUN and creatinine levels, renal inflammation, and tubular apoptosis.
*creat↓,

2512- H2,    Hydrogen Attenuates Allergic Inflammation by Reversing Energy Metabolic Pathway Switch
- in-vivo, Asthma, NA
selectivity↑, we treated mice with HRS for 7 days. HRS had no effects on OXPHOS and glycolytic activities in control mice
lactateProd↓, but prevented the elevation in lactate and reduction in ATP production in lungs of OVA-sensitized and challenged mice
ATP↑,
HK2↓, Consistently, HRS attenuated the increase in HK and PFK activities
PFK↓,
Hif1a↓, OVA sensitization and challenge increased HIF-1α nuclear translocation (stimulated HIF-1α activity), which was inhibited by HRS treatment
PGC-1α↑, By contrast, OVA sensitization and challenge downregulated PGC-1α protein expression, and HRS treatment reversed this downregulation
Glycolysis↓, H2 reverses energy metabolic switch by inhibiting glycolytic enzyme activities and by stimulating mitochondrial OXPHOS enzyme activities
OXPHOS↑,
Dose↝, HRS was prepared by dipping a plastic-shelled stick consisting of metallic magnesium (99.9% pure) and natural stones (Doctor SUISOSUI, Friendear Inc., Tokyo, Japan) into sterilized saline.

3767- H2,    The role of hydrogen therapy in Alzheimer's disease management: Insights into mechanisms, administration routes, and future challenges
- Review, AD, NA
*Inflam↓, Hydrogen therapy AD: inflammation, energy regulation, prevents neuronal damage.
*neuroP↑,
*toxicity↓, Hydrogen therapy's low side effects make it a complement to AD treatment. Even at high concentrations, hydrogen gas is still non-toxic, and has been widely used in the diving field.
*antiOx↑, hydrogen’s role as a natural antioxidant,
*ROS↓, Hydrogen has been shown to mitigate the amount of ROS released from mitochondria, thereby reducing mitochondrial DNA peroxidation and inhibiting the expression of NOD-like receptor thermal protein domain associated protein 3 (NLRP3), caspase-1, and I
*NLRP3↓,
*IL1β↓,
*mtDam↓, curtail mitochondrial damage, thereby bolstering ATP synthesis and fortifying the electron transport chain within mitochondria
*ATP↑,
*AMPK↑, activating AMPK and amplifying the downstream antioxidant response of forkhead box O3a (FOXO3
*FOXO3↑,
*SOD1↑, It elevates the levels of intracellular antioxidant enzymes, notably superoxide dismutase 1 (SOD1) and catalase (CAT), thereby serving as a neuroprotective agent that diminishes the risk and progression of AD
*Catalase↑,
*NRF2↑, Hydrogen slows AD progression by activating the cellular endogenous antioxidant system Nrf2;
*NO↓, Reduced inflammatory markers such as ROS, Nitric oxide (NO) and Malondialdehyde (MDA)
*MDA↓,
*lipid-P↓, drinking HRW significantly reduced lipid peroxidation in the brain of SAMP8 mice.
*memory↑, HRW inhibited the decline of learning and memory impairment
*ER(estro)↓, Decreased hormone levels, estrogen receptor (ER) β, and BDNF expression improve cognitive function in female transgenic AD mice.
*BDNF↑, upsurge in BDNF levels, which further ameliorated the cognitive impairments observed in mice affected by sepsis.
*cognitive↑,
*APP↓, The expression of APP, BACE1, and SAPPβ was proficiently suppressed, thereby curtailing the overproduction of Aβ in Alzheimer's
*BACE/β-secretase↓,
*Aβ↓,
*BP∅, inhaling hydrogen gas has no effect on blood pressure and other blood parameters (such as pH, body temperature, etc.),
*BBB↑, efficiently crossing the blood-brain barrier to perform their functions.

7503- H2S,    Hydrogen Sulfide, an Endogenous Stimulator of Mitochondrial Function in Cancer Cells
- Review, Var, NA
DNArepair↑, endogenous H2S in cancer cells include the maintenance of mitochondrial organization (protection against mitochondrial fission) and the maintenance of mitochondrial DNA repair
CBS↑, CBS is upregulated and H2S generation is increased in primary human colon cancer tissues compared to the surrounding (nominally healthy) tissues
3MST/MPST↑, it is now clear that CBS, and/or CSE and/or 3-MST is overexpressed in many forms of cancer.
ETC↑, H2S can enhance mitochondrial electron transport and ATP production in cancer cells are shown in Figure 1.
ATP↑,
Glycolysis↑, H2S can also stimulate glycolysis (another key energetic process in cancer cells
ACLY↑, recently discovered mechanism relates to the upregulation of ACLY by H2S

2887- HNK,    Honokiol Restores Microglial Phagocytosis by Reversing Metabolic Reprogramming
- in-vitro, AD, BV2
*Glycolysis↑, switch from oxidative phosphorylation to anaerobic glycolysis and enhancing ATP production.
*ATP↑,
*ROS↓, honokiol reduced mitochondrial reactive oxygen species production and elevated mitochondrial membrane potential.
*MMP↑,
*OXPHOS↑, Honokiol enhanced ATP production by promoting mitochondrial OXPHOS in BV2 cell
*PPARα↑, Therefore, we argue that honokiol increases the expression of PPAR and PGC1, thus regulating a metabolic switch from glycolysis to OXPHOS
*PGC-1α↑,

7636- Ins,    Myo-Inositol: Pharmacokinetics, Biological Functions, and Therapeutic Potential in Liver Protection: Insights from Preclinical Models
*glucose↝, Myo-inositol, the most common stereoisomer of inositol, plays an important role in many physiological processes, such as cell signaling, regulation of glucose and lipid metabolism, and protection of cells against oxidative stress.
*lipid-P↓,
*ROS↓,
*BioAv↑, characterized by high oral bioavailability and is primarily eliminated via the kidneys.
*hepatoP↑, Preclinical studies have shown that myo-inositol has hepatoprotective potential, reducing oxidative stress, inflammation, and lipid accumulation in hepatocytes,
*Inflam↓,
*MMP↑, Recent findings suggest that it contributes to the stabilization of mitochondrial membranes and enhances ATP production efficiency,
*ATP↑,
*GutMicro↑, Evidence indicates that myo-inositol may influence intestinal microbiota composition, enhancing populations of beneficial bacterial strains while reducing endotoxemia linked to non-alcoholic fatty liver disease
*Dose↝, a significant portion of the body’s requirement is also supplied by the diet-rich sources, including fruits, whole grains, legumes, and nuts.
*Half-Life↝, Studies on rats has revealed that the highest plasma concentrations were observed within 1–2 h after oral intake, while the half-life ranged from 4 to 8 h.
*BioAv↑, In the case of intravenous administration, higher bioavailability and faster tissue distribution were achieved. intravenous administration of myo-inositol is rare
*eff↑, myo-inositol supplementation may potentially synergize with antioxidants (e.g., vitamin E, curcumin), enhancing their protective effects on the liver and other organs exposed to oxidative stress
*hepatoP↑, Myo-inositol may exert hepatoprotective effects through several biological mechanisms. A key role is played by its involvement in lipid metabolism regulation, modulation of oxidative stress, and influence on insulin signaling.
*SOD↑, Moreover, myo-inositol and its derivatives (including D-chiro-inositol) affect the activation of antioxidant enzymes such as superoxide dismutase (SOD) and catalase, thereby limiting oxidative damage to hepatocytes
*Catalase↑,
*Casp3↓, inhibit the expression of apoptosis markers such as caspase-3,
*ALAT↓, decreased activity of transaminases (ALT, AST).
*AST↓,
*AMPK↑, regulation of lipid metabolism through the activation of AMP-activated protein kinase (AMPK) and downregulation of sterol regulatory element-binding proteins (SREBPs).
*SREBP1/SREBF1↑,
*NA↑,

7755- ISL,    Isoliquiritigenin attenuated cognitive impairment, cerebral tau phosphorylation and oxidative stress in a streptozotocin-induced mouse model of Alzheimer's disease
- in-vivo, AD, NA
*memory↑, Isoliquiritigenin treatment mitigated the spatial memory capacity of streptozotocin-injected mice and alleviated tau phosphorylation at Ser396 and Thr231,
*p‑T-cadherin↓,
*ROS↓, the production of reactive oxygen species, the intracellular ATP level, the mitochondrial proteins p-DRP1 (S616), Mfn1 and Mfn2, neuronal loss, and synaptic impairment
*ATP↑,
*p‑DRP1/DNM1L↝,
*MFN1↝,
*MFN2↝,
*neuroP↑,
*cognitive↑, In conclusion, our findings suggest that isoliquiritigenin ameliorates streptozotocin-induced cognitive impairment, hyperphosphorylated tau, oxidative stress, mitochondrial dysfunction and synaptic impairment
*mTOR↓, by decreasing mTOR and ERK activity and increasing GSK-3β activity.
*ERK↓,
*GSK‐3β↑,

7816- ISQ,    Isoquercitrin Induces Endoplasmic Reticulum Stress and Immunogenic Cell Death in Gastric Cancer Cells
- in-vitro, GC, AGS - in-vitro, GC, HGC27
TumCP↑, Isoquercitrin at doses greater than 20 μM had significant inhibitory effects on the survival of GC cell lines, including HGC-27, AGS, MKN-45, and SNU-1.
Bcl-2↓, downregulation of BCL-2 and upregulation of BAX, cleaved caspase-3, and caspase-12.
BAX↑,
cl‑Casp3↑,
Casp12↑,
MMP↓, isoquercitrin promoted the disruption of mitochondrial membrane potential in GC cells.
CRT↑, GC cell surface levels of calreticulin (CRT) and extracellular levels of CRT, ATP, and HMGB1 were enhanced by treatment with isoquercitrin.
e-ATP↑,
HMGB1↑,
HSP70/HSPA5↑, The protein levels of HMGB1, HSP70, and HSP90 were upregulated by isoquercitrin in a dose-dependent manner.
HSP90↑,
ER Stress↑, isoquercitrin induces ER stress and ICD in GC cells.

4292- LT,    Luteolin for neurodegenerative diseases: a review
- Review, AD, NA - Review, Park, NA - Review, MS, NA - Review, Stroke, NA
*Inflam↓, luteolin, showing significant anti-inflammatory, antioxidant, and neuroprotective activity.
*antiOx↑,
*neuroP↑,
*BioAv↝, To increase the bioavailability of luteolin, several delivery methods have been developed; the most thoroughly studied include lipid carriers like liposomes and nanoformulations
*BBB↑, luteolin given intraperitoneally (ip) to mice can readily cross the blood-brain barrier (BBB) and enter the brain
*TNF-α↓, nhibiting pro-inflammatory mediators such as cyclooxygenase-2 (COX-2), nitric oxide (NO), TNF-α, IL-β, IL-6, IL-8, IL-31, and IL-33 in several in vitro models of AD
*IL1β↓,
*IL6↓,
*IL8↓,
*IL33↓,
*NF-kB↓, inhibition of the NF-кB pathway
*BACE/β-secretase↓, leads to the inhibition of a downstream target– β-site amyloid precursor protein cleaving enzyme (BACE1), which is a key mediator in forming Aβ fibrils in AD pathology
*ROS↓, anti-oxidant activity mainly by reducing ROS levels and increasing SOD activity in in vitro models of AD
*SOD↑,
*HO-1↑, increase the expression of antioxidant enzymes such as heme oxygenase-1 (HO-1) via the nuclear factor erythroid 2–related factor 2/ antioxidant responsive element (Nrf-2/ARE) complex activation
*NRF2↑,
*Casp3↓, reducing the levels of caspase-3 and − 9 and improving the B-cell lymphoma protein 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, as it was reported in in vitro models of AD
*Casp9↑,
*Bax:Bcl2↓,
*UPR↑, enhancing the unfolded protein response (UPR) pathway, leading to an increase in endoplasmic reticulum (ER) chaperone GRP78 and a decrease in the expression of UPR-targeted pro-apoptotic genes via the MAPK pathway.
*GRP78/BiP↑,
*Aβ↓, evidence that suggests that luteolin can directly influence the formation of Aβ plaques by selectively inhibiting the activity of N-acetyl-α-galactosaminyltransferase (ppGalNAc-T) isoforms
*GSK‐3β↓, inactivating the glycogen synthase kinase-3 alpha (GSK-3α) isoform, suppressing Aβ and promoting tau disaggregation
*tau↓,
*CREB↑, luteolin promoted phosphorylation and activation of cAMP response element-binding protein (CREB) leading to the increased miR-132 expression, and eventually neurite outgrowth in PC12 cells
*ATP↑, ROS production was decreased by 40%, MMP levels were restored close to control N2a levels (202%), and ATP levels were improved by 444%).
*cognitive↑, protective effect of luteolin against cognitive dysfunction was also reported in the streptozotocin
*BloodF↑, Luteolin increased regional cerebral blood flow values, alleviated the leakage of the lumen of vessels, and protected the integrity of BBB
*BDNF↑, increasing the level of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor (TrkB) expression in the cerebral cortex
*TrkB↑,
*memory↑, luteolin supplementation significantly ameliorated memory and cognitive deficits in 3 × Tg-AD mice.
*PPARγ↑, attenuated mitochondrial dysfunction via peroxisome proliferator-activated receptor gamma (PPARγ) activation.
*eff↑, combination of luteolin with another compound– l-theanine (an amino acid found in tea) also improved AD-like symptoms in the Aβ25–35-treated rats

2643- MCT,    Medium Chain Triglycerides enhances exercise endurance through the increased mitochondrial biogenesis and metabolism
- Review, Nor, NA
*Akt↑, increased mitochondrial biogenesis and metabolism is mediated through the activation of Akt and AMPK signaling pathways and inhibition of TGF-β signaling pathway.
*AMPK↓,
*TGF-β↓, MCT downregulates TGF-β signaling
eff↑, beneficial effect of dietary MCT in exercise performance through the increase of mitochondrial biogenesis and metabolism.
*BioEnh↑, Furthermore, addition of the combination of chilli and MCT to meals increased diet-induced thermogenesis by over 50% in heathy normal-weight humans
*ATP↑, a key regulator of energy metabolism and mitochondrial membrane ATP synthase (ATP5α) were significantly upregulated by MCT.
*PGC-1α↑, also observed a significant increase in protein level of PGC-1α and ATP5α
*p‑mTOR↑, increased levels in both total and phosphorylated Akt and mTOR
*SMAD3↓, a compensatory response of the huge reduction in Smad3.

1780- MEL,    Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing
- Review, Var, NA
*antiOx↑, Melatonin is a potent antioxidant and antiageing molecule, is nontoxic, and enhances the efficacy and reduces the side effects of chemotherapy.
*toxicity↓,
ChemoSen↑,
*eff↑, melatonin was superior in preventing free radical destruction compared to other antioxidants, vitamin E, β-carotene, vitamin C, and garlic oil
*mitResp↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ATP↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ROS↓, most attractive property of melatonin is that its metabolites also regulate the mitochondrial redox status by scavenging ROS and RNS
*CardioT↓, melatonin has a protective effect on the heart without affecting DOX's antitumor activity,
*GSH↑, improving the de novo synthesis of glutathione (GSH) by promoting the activity of gamma-glutamylcysteine synthetase
*NOS2↓, melatonin inhibits the production of nitric oxide synthase (NOS)
*lipid-P↓, lipid peroxidation was reduced after melatonin treatment (role in induces organ failure)
eff↑, but it also enhances its antitumor activity more than vitamin E
*HO-1↑, melatonin upregulates heme oxygenase-1 (HO-1) (role in induces organ failure)
*NRF2↑, decreased bladder injury and apoptosis due to the upregulation of Nrf2 and nuclear transcription factor NF-κB expression
*NF-kB↑,
TumCP↓, significantly reduced cell proliferation
eff↑, Pretreatment with melatonin effectively preserved the ovaries from cisplatin-induced injury
neuroP↑, Melatonin has neuroprotective roles in oxaliplatin-induced peripheral neuropathy

1778- MEL,    Melatonin: a well-documented antioxidant with conditional pro-oxidant actions
- Review, Var, NA - Review, AD, NA
*ROS↓, melatonin and its metabolic derivatives possess strong free radical scavenging properties.
*antiOx↓, potent antioxidants against both ROS (reactive oxygen species) and RNS (reactive nitrogen species). reduce oxidative damage to lipids, proteins and DNA under a very wide set of conditions where toxic derivatives of oxygen are known to be produced.
ROS↑, a few studies using cultured cells found that melatonin promoted the generation of ROS at pharmacological concentrations (μm to mm range) in several tumor and nontumor cells; thus, melatonin functioned as a conditional pro-oxidant.
selectivity↑, melatonin functions as a prooxidant in cancer cells where it aids in the killing of tumor cells
Dose↑, Melatonin levels in the nucleus and mitochondria reached saturation with a lower dose of 40 mg/kg body weight, with no further accumulation under higher doses of injected melatonin
*mitResp↑, improves mitochondrial respiration and ATP production, thereby reducing electron leakage and ROS generation
*ATP↑,
*ROS↓,
eff↑, melatonin protects mitochondrial function in the brain of Alzheimer's patients through both MT1/MT2 dependent and independent mechanisms
ROS↑, Cytochrome P450 utilizes melatonin as a substrate to generate ROS in mitochondria (melatonin concentration ranges from 0.1 to 10 uM)
Dose↑, melatonin at high concentrations (10-1000uM ) was able to promote ROS generation and lead to Fas-induced apoptosis in human leukemic Jurkat cells. Concentrations of <10uM , melatonin did not induce significant ROS generation in these cancer cells
*toxicity∅, High levels of melatonin (uM to mM) did not cause cytotoxicity in several types of nontumor cells
ROS↑, lower concentrations of melatonin (0.1-10uM ), which exhibited antioxidant action in HepG2 cells within 24 hr, became pro-oxidant after 96 hr of treatment, as indicated by the increase of GSH with 24hr and depletion after 96 hr.
eff↓, Finally, a compound, chlorpromazine, which specifically interrupts the binding of melatonin to calmodulin [188], prevented melatonin-induced AA release and ROS generation;
ROS↝, It remains unknown whether the pro-oxidant action exists in vivo. the vast majority of evidence indicates that melatonin is a potent antioxidant in vivo even at pharmacological concentrations
Dose↑, decline of melatonin production with age may render it more beneficial to supplement melatonin to the aging population to improve health by reducing free radical damage
other↑, melatonin intake has the potential to improve cardiac function, inhibit cataract formation, maintain brain health, alleviate metabolic syndrome, obesity and diabetes,reduce tumorigenesis, protect tissues against ischemia

6419- MEL,    The potential influence of melatonin on mitochondrial quality control: a review
- Review, Nor, NA
*mt-ACC⇅, Melatonin regulates pyruvate or fatty acid metabolism to increase the concentration of acetyl-CoA in mitochondria. these studies indicate that melatonin increases or decreases acetyl-CoA content in mitochondria to regulate mitochondrial metabolism.
*PKM1↑, melatonin increases the activity of pyruvate kinase M1/2 (PKM) to regulate glycolysis
*PKM2↑,
*Glycolysis↝,
*PDKs↑, melatonin activates pyruvate dehydrogenase kinase 4 (PDK4) to regulate acetyl-CoA content
*FAO↑, melatonin can promote fatty acid metabolism by directly enhancing β-oxidation or increasing the transfer of fatty acid-derived acetyl-CoA into mitochondria
*ETC↑, Second, melatonin can enhance the activity of the electron-transport chain (ETC) and oxidative phosphorylation (OXPHOS) to regulate mitochondrial metabolism.
*OXPHOS↑,
*ATP↑, melatonin enhanced OXPHOS and promoted adenosine triphosphate (ATP) synthesis in rat brain and liver mitochondria
Glycolysis↓, ome studies have found that melatonin drove the switch from cytosolic glycolysis to mitochondrial OXPHOS in cancer cells
OXPHOS↑,
*Ca+2↓, melatonin can regulate the membrane potential of mitochondria and decrease excessive calcium levels to enhance ETC activity to increase ATP production
*ROS↓, Melatonin exhibits superior antioxidant ability. Melatonin, as a major scavenger of reactive oxygen species (ROS), may play a pivotal role in protecting mitochondria from ROS-induced injury
*antiOx↑, These specific characteristics make melatonin a broad-spectrum antioxidant.
*SOD2↑, melatonin can upregulate the expression of superoxide dismutase (MnSOD), glutathione peroxidase (GSH-Px) and catalase (CAT) to prevent cell stress and injury
*GPx↑,
*Catalase↑,
*MFN1↑, On the one hand, melatonin increases mitochondrial fusion-related genes such as mitofusin-1 (Mfn1), mitofusin-2 (Mfn2) and optic atrophy1 (Opa1) to promote mitochondrial fusion
*MFN2↑,
*OPA1↑,
*YAP/TEAD↑, studies have found that melatonin activated the Yap-Hippo pathway to increase Opa1-related fusion
*Hippo↑,
*SIRT1↑, melatonin alleviated cardiac dysfunction induced by diabetes by upregulating SIRT1-PGC1α to inhibit the expression of Drp1
*PGC-1α↑,
*DRP1/DNM1L↓,

2247- MF,    Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis
- in-vivo, Nor, NA
*Glycolysis↓, PEMF-treated animals exhibited decreased glycolysis and increased LDHB expression, enhancing NAD signaling and ATP production
*LDHB↑,
*NAD↑,
*ATP↑,
*antiOx↑, Antioxidant protein levels increased, controlling ROS production.
*ROS↑,
*YAP/TEAD↑, upregulation of YAP and PGC1alpha and increasing slow myosin isoforms, thus speeding up physiological recovery.
*PGC-1α↑,
*TCA↑, increased in PEMF-treated injured limbs
*FAO↑,
*OXPHOS↑, Oxidative phosphorylation was increased in the muscle of injured rats that underwent PEMF treatment

4355- MF,    Ambient and supplemental magnetic fields promote myogenesis via a TRPC1-mitochondrial axis: evidence of a magnetic mitohormetic mechanism
- in-vitro, Nor, C2C12
*mt-OCR↑, figure 1
*mt-ROS↑, Exposure to PEMFs stimulated the production of ROS (Fig. 6A, B) and ATP
*ECAR↑, figure 6
*Dose↝, barrages of 20 × 150 μs on and off pulses for 6 ms repeated at a frequency of 15 Hz. The magnetic flux density rose to predetermined maximal level within ∼50 μs (∼17 T/s) when driving field amplitudes between 0.5 and 3 mT.
*Ca+2↑, 10 min) of C2C12 myoblasts to PEMFs (Supplemental Fig. S1A) augmented cytosolic calcium levels [intracellular [Ca2+] concentration ([Ca2+]i), blue] relative to unexposed myoblasts
*ATP↑,
*other↑, PEMF-stimulated proliferation of myoblasts
*eff↓, TRPC1 silencing precludes PEMF sensitivity.
*eff↝, revealed a magnetic efficacy window

538- MF,    The extremely low frequency electromagnetic stimulation selective for cancer cells elicits growth arrest through a metabolic shift
- in-vitro, BC, MDA-MB-231 - in-vitro, Melanoma, MSTO-211H
TumCG↓, did not affect the non-malignant counterpart.
Ca+2↑,
COX2/PTGS2↓,
ATP↑, (ATP5B) and mitochondrial transcription (MT-ATP6)
MMP↑, significant enhancement of mitochondrial membrane potential (ΔΨm)
ROS↑, demonstrated for the first time the association of ROS production with the stimulation of the mitochondrial metabolism triggered by the electromagnetic field
OXPHOS↑,
mitResp↑, Mitochondrial respiration is increased by ELF-EMF exposure

493- MF,    Extremely low-frequency electromagnetic field induces acetylation of heat shock proteins and enhances protein folding
- in-vitro, NA, HEK293 - in-vitro, Liver, AML12
ATP↑,
HSP70/HSPA5↓, however, acetylations of HSP70 and HSP90 were increased
HSP90↓, however, acetylations of HSP70 and HSP90 were increased

3477- MF,    Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis
- Review, NA, NA
*Ca+2↑, When cells are subjected to external mechanical stimulation, voltage-gated ion channels in the cell membrane open and intracellular calcium ion concentration rises
*VEGF↑, BMSCs EMF combined with VEGF promote osteogenesis and angiogenesis
*angioG↑,
Ca+2↑, 1 Hz/100 mT MC4-L2 breast cancer cells EMF lead to calcium ion overload and ROS increased, resulting in necroptosis
ROS↑,
Necroptosis↑,
TumCCA↑, 50 Hz/4.5 mT 786-O cells ELF-EMF induce G0/G1 arrest and apoptosis in cells lines
Apoptosis↑,
*ATP↑, causing the ATP or ADP increases, and the purinergic signal can upregulate the expression of P2Y1 receptors
*FAK↑, Our research team [53] found that ELE-EMF can induce calcium oscillations in bone marrow stem cells, up-regulated calcium ion activates FAK pathway, cytoskeleton enhancement, and migration ability of stem cells in vitro is enhanced.
*Wnt↑, ability of EMF to activate the Wnt10b/β-catenin signaling pathway to promote osteogenic differentiation of cells depends on the functional integrity of primary cilia in osteoblasts.
*β-catenin/ZEB1↑,
*ROS↑, we hypothesize that the electromagnetic field-mediated calcium ion oscillations, which causes a small amount of ROS production in mitochondria, regulates the chondrogenic differentiation of cells, but further studies are needed
p38↑, RF-EMF was able to suppress tumor stem cells by activating the CAMKII/p38 MAPK signaling pathway after inducing calcium ion oscillation and by inhibiting the β-catenin/HMGA2 signaling pathway
MAPK↑,
β-catenin/ZEB1↓,
CSCs↓, Interestingly, the effect of electromagnetic fields is not limited to tumor stem cells, but also inhibits the proliferation and development of tumor cells
TumCP↓,
ROS↑, breast cancer cell lines exposed to ELE-EMF for 24 h showed a significant increase in intracellular ROS expression and an increased sensitivity to further radiotherapy
RadioS↑,
Ca+2↑, after exposure to higher intensity EMF radiation, showed a significant increase in intracellular calcium ion and reactive oxygen species, which eventually led to necroptosis
eff↓, while this programmed necrosis of tumor cells was able to be antagonized by the calcium blocker verapamil or the free radical scavenger n -acetylcysteine
NO↑, EMF can regulate multiple ions in cells, and calcium ion play a key role [92, 130], calcium ion acts as a second messenger that can activate downstream molecules such as NO, ROS

3350- QC,    Quercetin and the mitochondria: A mechanistic view
- Review, NA, NA
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*NRF2↑, Quercetin is able to activate the master regulator nuclear factor erythroid 2-related factor 2 (Nrf2)
ROS⇅, That is, as a free radical-scavenging antioxidant, quercetin protects cells against DNA damage induced by reactiveoxygen species (ROS), but the oxidized quercetin intermediates (see above) can then react with glutathione (GSH) thereby lowering GSH
*NRF2↑, 10uM (24 h) Mouse primary hepatocytes Activation of Nrf2; ↑HO-1 levels; ↑expression of PPARα and PGC-1α
*HO-1↑,
*PPARα↑,
*PGC-1α↑,
*SIRT1↑, Rat hippocampus ↑ SIRT1, PGC-1α, NRF-1, and TFAM levels; ATP levels;
*ATP↑,
ATP↓, L1210 and P388 leukemia cells (Suolinna et al., 1975). At least in part, the authors attributed the pro-apoptotic effect of quercetin in these cell lines to its capacity to inhibit ATP synthase, causing a decrease in ATP content.
ERK↓, downregulation of ERK1/2 by quercetin (50-100 uM for 24 or 48 h, combined or not with resveratrol
cl‑PARP↑, NCaP cells ↑PARP cleavage ↑ Caspase-9, caspase-8, and caspase-3 activities
Casp9↑,
Casp8↑,
BAX↑, MDA-MB-231 cells ↑Bax levels, ↓MMP, ↑cytochrome c release, ↑caspase-9 and caspase-3 activities
MMP↓,
Cyt‑c↑,
Casp3↑,
HSP27↓, T98G cells: ↓Hsp27 and Hsp72 contents, ↓Ras and Raf level
HSP72↓,
RAS↓,
Raf↓,

3336- QC,    Neuroprotective Effects of Quercetin in Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, Neuroprotection by quercetin has been reported in several in vitro studies
*lipid-P↓, It has been shown to protect neurons from oxidative damage while reducing lipid peroxidation.
*antiOx↑, In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways.
*Aβ↓,
*Inflam↓,
*BBB↝, It also has low BBB penetrability, thus limiting its efficacy in combating neurodegenerative disorders.
*NF-kB↓, downregulating pro-inflammatory cytokines, such as NF-kB and iNOS, while stimulating neuronal regeneration
*iNOS↓,
*memory↑, Quercetin has shown therapeutic efficacy, improving learning, memory, and cognitive functions in AD
*cognitive↑,
*AChE↓, Quercetin administration resulted in the inhibition of AChE
*MMP↑, quercetin ameliorates mitochondrial dysfunction by restoring mitochondrial membrane potential, decreases ROS production, and restores ATP synthesis
*ROS↓,
*ATP↑,
*AMPK↑, It also increased the expression of AMP-activated protein kinase (AMPK), which is a key cell regulator of energy metabolism.
*NADPH↓, Activated AMPK can decrease ROS generation by inhibiting NADPH oxidase activity
*p‑tau↓, Inhibition of AβAggregation and Tau Phosphorylation

2566- RES,    A comprehensive review on the neuroprotective potential of resveratrol in ischemic stroke
- Review, Stroke, NA
*neuroP↑, comprehensive overview of resveratrol's neuroprotective role in IS
*NRF2↑, Findings from previous studies suggest that Nrf2 activation can significantly reduce brain injury following IS and lead to better outcomes
*SIRT1↑, neuroprotective effects by activating nuclear factor erythroid 2-related factor 2 (NRF2) and sirtuin 1 (SIRT1) pathways.
*PGC-1α↑, IRT1 activation by resveratrol triggers the deacetylation and activation of downstream targets like peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) and forkhead box protein O (FOXO)
*FOXO↑,
*HO-1↑, ctivation of NRF2 through resveratrol enhances the expression of antioxidant enzymes, like heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), which neutralize reactive oxygen species and mitigate oxidative stress in the ischemic bra
*NQO1↑,
*ROS↓,
*BP↓, Multiple studies have demonstrated that resveratrol presented protective effects in IS, it can mediate blood pressure and lipid profiles which are the main key factors in managing and preventing stroke
*BioAv↓, The residual quantity of resveratrol undergoes metabolism, with the maximum reported concentration of free resveratrol being 1.7–1.9 %
*Half-Life↝, The levels of resveratrol peak 60 min following ingestion. Another study found that within 6 h, there was a further rise in resveratrol levels. This increase can be attributed to intestinal recirculation of metabolites
*AMPK↑, Resveratrol also increases AMPK and inhibits GSK-3β (glycogen synthase kinase 3 beta) activity in astrocytes, which release energy, makes ATP available to neurons and reduces ROS
*GSK‐3β↓,
*eff↑, Furthermore, oligodendrocyte survival is boosted by resveratrol, which may help to preserve brain homeostasis following a stroke
*AntiAg↑, resveratrol may suppress platelet activation and aggregation caused by collagen, adenosine diphosphate, and thrombin
*BBB↓, Although resveratrol is a highly hydrophobic molecule, it is exceedingly difficult to penetrate a membrane like the BBB. However, an alternate administration is through the nasal cavity in the olfactory area, which results in a more pleasant route
*Inflam↓, Resveratrol's anti-inflammatory effects have been demonstrated in many studies
*MPO↓, Resveratrol dramatically lowered the amounts of cerebral infarcts, neuronal damage, MPO activity, and evans blue (EB) content in addition to neurological impairment scores.
*TLR4↓, TLR4, NF-κB p65, COX-2, MMP-9, TNF-α, and IL-1β all had greater levels of expression after cerebral ischemia, whereas resveratrol decreased these amounts
*NF-kB↓,
*p65↓,
*MMP9↓,
*TNF-α↓,
*IL1β↓,
*PPARγ↑, Previous studies have shown that resveratrol activates the PPAR -γ coactivator 1α (PGC-1 α), which has free radical scavenging properties
*MMP↑, Resveratrol can prevent mitochondrial membrane depolarization, preserve adenosine triphosphate (ATP) production, and inhibit the release of cytochrome c
*ATP↑,
*Cyt‑c∅,
*mt-lipid-P↓, mitochondrial lipid peroxidation (LPO), protein carbonyl, and intracellular hydrogen peroxide (H2O2) content were significantly reduced in the resveratrol treatment group, while the expression of HSP70 and metallothionein were restored
*H2O2↓,
*HSP70/HSPA5↝,
*Mets↝,
*eff↑, Shin et al. showed that 5 mg/kg intravenous (IV) resveratrol reduced infarction volume by 36 % in an MCAO mouse model.
*eff↑, This study indicates that resveratrol holds the potential to improve stroke outcomes before ischemia as a pre-treatment strategy
*motorD↑, resveratrol treatment significantly reduced infarct volume and prevented motor impairment, increased glutathione, and decreased MDA levels compared to the control group,
*MDA↓,
*NADH:NAD↑, Resveratrol treatment significantly enhanced the intracellular NAD+/NADH ratio
eff↑, Pretreatment with resveratrol (20 or 40 mg/kg) significantly lowered the cerebral edema, infarct volume, lipid peroxidation products, and inflammatory markers
eff↑, Intraperitoneal administration of resveratrol at a dose of 50 mg/kg reduced cerebral ischemia reperfusion damage, brain edema, and BBB malfunction

993- RES,    Resveratrol reverses the Warburg effect by targeting the pyruvate dehydrogenase complex in colon cancer cells
- in-vitro, CRC, Caco-2 - in-vivo, Nor, HCEC 1CT
TumCG↓,
Glycolysis↓,
PPP↓,
ATP↑, significant increase (20%) in ATP production
PDH↑, Resveratrol targets the pyruvate dehydrogenase (PDH) complex, a key mitochondrial gatekeeper of energy metabolism, leading to an enhanced PDH activity.
Ca+2↝, resveratrol is a potent modulator of many cellular Ca2+ signaling pathways. Ca2+ is a key mediator of the effect of resveratrol on the oxidative capacity of colon cancer cells.
TumCP↓,
lactateProd↓,
OCR↑, increase of oxygen consumption rate (OCR) both in normal colonic epithelial HCEC 1CT cells
ECAR↓, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells, whereas it was significantly reduced (31%) in HCEC 1CT RPA cells ****
*ECAR∅, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells
*other?, Resveratrol promotes a shift from respiration to glycolysis in cancer-like cells, but not in normal colonocytes
cycE/CCNE↑, Resveratrol inhibited cell cycle progression by enhancing the levels of cyclin E and cyclin A
cycA1/CCNA1↑,
TumCCA↑,
cycD1/CCND1↑, and by decreasing cyclin D1
OXPHOS↑, Taken together, these observations indicate that exposure to resveratrol leads to a metabolic reorientation from aerobic glycolysis toward OXPHOS.

6420- RES,    Resveratrol Regulates Mitochondrial Biogenesis and Fission/Fusion to Attenuate Rotenone-Induced Neurotoxicity
- in-vivo, Park, NA
*DRP1/DNM1L↑, resveratrol pretreatment could improve the ability of mitochondrial fission and fusion, by promoting expression of Drp1, Fis1, OPA1, and MFN2 mRNA and protein associated with mitochondrial fission and fusion
*FIS1↑,
*OPA1↑,
*MFN2↑,
*motorD↑, resveratrol pretreatment decreased the disturbance of motor coordination, with the rate and duration of motion enhanced significantly.
*PGC-1α↑, Moreover, resveratrol pretreatment could reverse the inhibition of PGC-1α and mtTFA protein and mRNA expression caused by rotenone
*ROS↓, if PC12 cells were pretreated with resveratrol, the ROS production decreased (Figure 5(a)) and ATP production (Figure 5(b)) increased significantly
*ATP↑,

6423- RES,    Resveratrol Regulates Mitochondrial Biogenesis and Fission/Fusion to Attenuate Rotenone-Induced Neurotoxicity
- vitro+vivo, Park, NA
*neuroP↑, resveratrol may prevent rotenone-induced neurotoxicity through regulating mitochondrial fission/fusion and biogenesis.
*FIS1↓, Fis1, OPA1, and MFN2 protein and mRNA levels involved in mitochondrial fission and fusion reveals a significant decrease in the R groups compared with the control group
*OPA1↓,
*MFN2↓,
*PGC-1α↑, Resveratrol pretreatment significantly increased protein and mRNA expression of PGC-1α and mtTFA
*ROS↓, if PC12 cells were pretreated with resveratrol, the ROS production decreased (Figure 5(a)) and ATP production (Figure 5(b)) increased significantly
*ATP↑,
*motorD↑, resveratrol could significantly ameliorate the motor dysfunction

3729- RF,    Review of the Evidence that Transcranial Electromagnetic Treatment will be a Safe and Effective Therapeutic Against Alzheimer's Disease
- in-vivo, AD, NA
*cognitive↑, demonstrated in multiple studies that daily, long-term electromagnetic field (EMF) treatment in the ultra-high frequency range not only protects Alzheimer’s disease (AD) transgenic mice from cognitive impairment, but also reverses such impairment in
*Aβ↓, daily EMF treatment over months reversed both cognitive impairment (Fig. 2A) and Aβ deposition
*ROS↓, fig 5
*ATP↑,

3733- RF,    Long-term electromagnetic field treatment enhances brain mitochondrial function of both Alzheimer's transgenic mice and normal mice: a mechanism for electromagnetic field-induced cognitive benefit?
- in-vivo, AD, NA
*Aβ↓, ability of EMF treatment to disaggregate Aβ oligomers, which are believed to be the form of Aβ causative to mitochondrial dysfunction in Alzheimer's disease (AD).
*cognitive↑, EMF treatment provides cognitive benefit to both Tg and NT mice
*mt-ROS↓, fig 4
*ATP↑, EMF treatment increases mitochondrial ATP levels selectively in Tg mice


Showing Research Papers: 1 to 50 of 63
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 63

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

3MST/MPST↑, 1,   BHB↑, 1,   CBS↑, 1,   CD47↓, 1,   HMGCS2↑, 1,   miR-124-3p↓, 1,   PFS↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   GSTs↑, 1,   HO-1↓, 1,   lipid-P↓, 1,   OXPHOS↓, 1,   OXPHOS↑, 5,   ROS↓, 1,   ROS↑, 9,   ROS⇅, 1,   ROS↝, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 2,   ATP↑, 6,   e-ATP↑, 1,   i-ATP↑, 1,   ETC↑, 1,   Insulin↓, 1,   mitResp↓, 1,   mitResp↑, 1,   MMP↓, 2,   MMP↑, 1,   OCR↓, 1,   OCR↑, 1,   PGC-1α↑, 2,   Raf↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACLY↑, 1,   cMyc↓, 1,   ECAR↓, 2,   Glycolysis↓, 5,   Glycolysis↑, 1,   HK2↓, 1,   lactateProd↓, 2,   PDH↑, 1,   PFK↓, 1,   PPP↓, 1,   SCD1↓, 1,   SIRT1↑, 1,   Warburg↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 5,   Bak↓, 1,   BAX↑, 3,   Bcl-2↓, 2,   BID↑, 1,   Casp12↑, 1,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp8↑, 2,   Casp9↑, 3,   Cyt‑c↑, 3,   Fas↑, 1,   IAP2/BIRC3↓, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   Necroptosis↑, 1,   p38↑, 1,   TumCD↑, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,   ac‑H3↑, 1,   ac‑H4↑, 1,   other↑, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CRT↑, 1,   ER Stress↑, 1,   HSP27↓, 1,   HSP70/HSPA5↓, 1,   HSP70/HSPA5↑, 1,   HSP72↓, 1,   HSP90↓, 1,   HSP90↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG3↑, 1,   Beclin-1↑, 1,   LAMP2↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   DNArepair↑, 1,   P53↓, 1,   P53↑, 3,   PARP↑, 2,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   cycA1/CCNA1↑, 1,   cycD1/CCND1↓, 1,   cycD1/CCND1↑, 1,   cycE/CCNE↑, 1,   mitA↑, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CSCs↓, 1,   ERK↓, 2,   FGF↓, 1,   GSK‐3β↑, 1,   HDAC↓, 2,   IGF-1↓, 1,   PI3K↓, 1,   RAS↓, 1,   STAT5↓, 1,   TumCG↓, 3,   TumCG↑, 1,  

Migration(tgid=13) ⓘ

BACH1↓, 1,   Ca+2↑, 3,   Ca+2↝, 1,   i-Ca+2↑, 1,   CEA↓, 1,   LAMs↓, 1,   MALAT1↓, 1,   SPARC↑, 1,   TIMP2↑, 1,   Treg lymp↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 7,   TumCP↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   EGFR↑, 1,   Hif1a↓, 3,   NO↑, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 3,   HMGB1↑, 1,   pol-M1↑, 1,   M2 MC↓, 1,   pol-M2 MC↓, 1,   NF-kB↓, 2,   NF-kB↑, 1,   NK cell↑, 1,   p65↓, 1,   PD-1↓, 1,   PGE2↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 4,   Dose↑, 3,   Dose↝, 4,   eff↓, 3,   eff↑, 10,   RadioS↑, 2,   selectivity↑, 4,  

Clinical Biomarkers(tgid=22) ⓘ

BG↓, 1,   CEA↓, 1,   EGFR↓, 1,   EGFR↑, 1,   EZH2↓, 1,   GutMicro↑, 2,   HER2/EBBR2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   chemoP↑, 2,   ChemoSideEff↓, 1,   neuroP↑, 1,   NP/CIPN↓, 2,   QoL↑, 1,   radioP↑, 1,   RenoP↑, 1,   TumVol↓, 1,   Weight∅, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 3,  
Total Targets: 167

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 2,   compII↑, 1,   DA↑, 1,   diuretic↑, 1,   NA↑, 1,   Stroke↓, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 15,   Catalase↑, 11,   compI↑, 1,   GPx↑, 7,   GSH↑, 10,   GSR↓, 1,   H2O2↓, 2,   HO-1↓, 1,   HO-1↑, 7,   Keap1↑, 1,   Keap1↝, 1,   lipid-P↓, 10,   mt-lipid-P↓, 1,   MDA↓, 8,   Mets↝, 1,   MFN1↑, 1,   MFN1↝, 1,   MFN2↓, 1,   MFN2↑, 3,   MFN2↝, 1,   MPO↓, 2,   NQO1↑, 3,   NRF2↑, 12,   OPA1↓, 1,   OPA1↑, 2,   OXPHOS↑, 3,   Prx↓, 1,   ROS↓, 31,   ROS↑, 2,   mt-ROS?, 1,   mt-ROS↓, 1,   mt-ROS↑, 1,   SIRT3↑, 1,   SOD↑, 10,   SOD1↑, 1,   SOD2↑, 1,   TBARS↓, 1,   uricA↓, 1,   VitC↑, 1,   VitE↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 2,   ATP↑, 42,   compIII↑, 1,   DRP1/DNM1L↓, 1,   DRP1/DNM1L↑, 1,   p‑DRP1/DNM1L↝, 1,   ETC↑, 2,   FIS1↓, 2,   FIS1↑, 1,   Insulin↑, 1,   mitResp↑, 5,   MMP↑, 10,   mtDam↓, 3,   OCR↑, 1,   mt-OCR↑, 1,   PGC-1α↑, 9,   PGC-1α↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

mt-ACC⇅, 1,   ALAT↓, 4,   AMPK↓, 1,   AMPK↑, 5,   BUN↓, 1,   CREB↑, 1,   ECAR↑, 1,   ECAR∅, 1,   FAO↑, 3,   FASN↓, 1,   glucose↓, 2,   glucose↝, 1,   GlucoseCon↑, 1,   Glycolysis↓, 1,   Glycolysis↑, 1,   Glycolysis↝, 1,   KeyT↝, 1,   LDH↓, 1,   LDHB↑, 1,   LDL↓, 1,   NAD↑, 1,   NADH:NAD↑, 1,   NADPH↓, 1,   PDKs↑, 1,   PFK↓, 1,   PGM1?, 1,   PKM1↑, 1,   PKM2↓, 1,   PKM2↑, 1,   PPARα↑, 2,   PPARγ↑, 3,   SIRT1↑, 3,   SREBP1/SREBF1↑, 1,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 2,   Apoptosis↓, 3,   BAX↓, 1,   Bax:Bcl2↓, 1,   Bcl-2↑, 3,   Casp12↓, 1,   Casp3↓, 7,   Casp9↓, 3,   Casp9↑, 1,   Cyt‑c↓, 1,   Cyt‑c∅, 1,   GranB/GZMB↓, 1,   GSDMD↓, 1,   Hippo↑, 1,   iNOS↓, 6,   p‑JNK↓, 1,   p38↓, 1,   YAP/TEAD↑, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

TRPV3↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 2,   other?, 1,   other↑, 2,   other↝, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↝, 1,   UPR↑, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

PARP1↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,   FOXO↑, 1,   FOXO3↑, 1,   GSK‐3β↓, 4,   GSK‐3β↑, 1,   HDAC2↓, 1,   mTOR↓, 2,   p‑mTOR↑, 1,   Nestin↑, 1,   NOTCH1↑, 1,   PI3K↓, 1,   PI3K↑, 2,   SOX2↑, 1,   STAT↓, 1,   STAT3↑, 1,   Wnt↑, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   AntiAg↑, 2,   APP↓, 3,   Ca+2↓, 2,   Ca+2↑, 3,   FAK↑, 1,   Ki-67↑, 1,   MMP13↓, 1,   MMP9↓, 1,   PKA↑, 1,   SMAD3↓, 1,   p‑T-cadherin↓, 1,   TGF-β↓, 1,   TGF-β↑, 1,   VCAM-1↓, 2,   Vim↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   ATF4↓, 1,   eNOS↑, 1,   NO↓, 2,   NO↑, 1,   VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↓, 1,   BBB↑, 4,   BBB↝, 1,   GastroP↑, 2,   IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 2,   COX2/PTGS2↓, 6,   COX2/PTGS2↑, 1,   CRP↓, 1,   IFN-γ↓, 1,   IL10↑, 1,   IL18↓, 1,   IL1β↓, 9,   IL2↓, 2,   IL33↓, 1,   IL4↓, 2,   IL6↓, 7,   IL6↑, 1,   IL8↓, 1,   Imm↑, 2,   INF-γ↓, 1,   Inflam↓, 18,   LPS↓, 1,   pol-M2 MC↑, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 6,   NF-kB↑, 1,   p‑NF-kB↓, 1,   p65↓, 1,   PGE2↓, 2,   TLR4↓, 1,   TNF-α↓, 12,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 2,   AChE↓, 5,   BChE↓, 2,   BDNF↑, 5,   ChAT↑, 1,   MAOA↓, 2,   NGF↑, 2,   tau↓, 1,   p‑tau↓, 2,   TrkB↑, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 11,   BACE/β-secretase↓, 5,   MAOB↓, 1,   NLRP3↓, 2,   PP2A↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ER(estro)↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 8,   BioAv↝, 5,   BioEnh↑, 1,   Dose↝, 5,   eff↓, 2,   eff↑, 11,   eff↝, 1,   Half-Life↓, 1,   Half-Life↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 4,   AST↓, 4,   BloodF↑, 3,   BP↓, 2,   BP∅, 1,   creat↓, 3,   CRP↓, 1,   GutMicro↑, 4,   IL6↓, 7,   IL6↑, 1,   Ki-67↑, 1,   LDH↓, 1,   NOS2↓, 1,   Urea↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiDiabetic↑, 2,   antiPs↑, 2,   cardioP↑, 7,   CardioT↓, 1,   chemoP↑, 1,   chemoPv↑, 1,   cognitive↑, 16,   hepatoP↑, 7,   memory↑, 9,   Mood↑, 1,   motorD↑, 4,   neuroP↑, 20,   Obesity↓, 4,   Pain↓, 2,   RenoP↑, 3,   toxicity↓, 8,   toxicity∅, 1,   Weight↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 2,   Bacteria↓, 2,   CD8+↑, 1,   Diar↓, 1,   Sepsis↓, 3,  
Total Targets: 272

Scientific Paper Hit Count for: ATP, Adenosine triphosphate
5 Magnetic Fields
4 Hydrogen Gas
4 Resveratrol
4 Urolithin
3 Melatonin
2 Alpha-Lipoic-Acid
2 Crocetin
2 Curcumin
2 Ginkgo biloba-EGb 761
2 Ginkgo biloba
2 Luteolin
2 Quercetin
2 Rosmarinic acid
2 EGCG (Epigallocatechin Gallate)
2 Vitamin B5,Pantothenic Acid
1 Anthocyanins
1 Acetyl-l-carnitine
1 Ashwagandha(Withaferin A)
1 α-Bisabolol / Chamomile oil
1 Capsaicin
1 Carvacrol
1 Centella asiatica / Gotu kola → asiaticoside
1 Cichoric acid / Chicoric acid
1 Citric Acid
1 diet FMD Fasting Mimicking Diet
1 Chemotherapy
1 Emodin
1 Ferulic acid
1 Formononetin
1 Cisplatin
1 hydrogen sulfide
1 Honokiol
1 Inositol
1 Isoliquiritigenin
1 isoquercitrin
1 MCToil
1 Radio Frequency
1 EMF
1 Docosahexaenoic Acid
1 Vitamin B1/Thiamine
1 Vitamin B12
1 Folic Acid, Vit B9
1 Vitamin B2,Riboflavin
1 Vitamin K2
1 probiotics
1 Vitexin
1 Isovitexin
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:21  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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