Obesity Cancer Research Results
Obesity, Obesity: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
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*Dose↝, For four weeks, 100 and 10 mg/kg/day of EAO and isoquercitrin, respectively, were administered orally
*Obesity↓, Administration of EAO and isoquercitrin significantly decreased body weight in HFD and Aβ-injected mice
*Leptin↓, decrease in leptin and an increase in adiponectin levels compared with the control group
*adiP↑,
*hepatoP↑, EAO- and isoquercitrin-administered groups attenuated liver damage
*PSEN1/PS1↓, administration of EAO and isoquercitrin groups down-regulated amyloidosis-related proteins in the brain such as β-secretase, presenilin (PS)-1 and PS-2 compared with HFD and Aβ-injected mice.
*PSEN2/PS-2↓,
*BACE/β-secretase↓,
*eff↑, EAO and isoquercitrin attenuated HFD and Aβ-induced obesity and amyloidosis, suggesting that they could be effective in preventing and treating both obesity and AD.
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*AntiDiabetic↑, Through modulating oxidative stress, SIRT-1 expression, PPAR gamma receptors, and other multiple mechanisms biochanin-A produces anti-diabetic action.
*neuroP↑, Biochanin-A has been shown to have a potential neuroprotective impact by modulating multiple critical neurological pathways.
*toxicity↓, Unlike chemical agents such as chemotherapeutic agents, isoflavones have shown zero toxicity to humans
*CYP19↓, Biochanin-A inhibits CYP19 and negatively affects the synthesis of oestrogen in the body which enhances the anti-oestrogenic property in hormone-influenced cancer such as prostate cancer and breast cancer
p‑Akt↓, Biochanin-A inhibits Akt phosphorylation thereby downregulates mTOR signals and disrupts the cell cycle.
mTOR↓,
TumCCA↑,
P21↑, Biochanin-A cause apoptosis in lung cancer by increasing p21, caspase-3, and Bcl-2 levels. It lowers E-cadherin and blocks metastasis.
Casp3↑,
Bcl-2↑,
Apoptosis↑,
E-cadherin↓,
TumMeta↓,
eff↑, The synergism of biochanin-A with 5-fluorouracil evidenced in Caco-2 and HCT-116 cell lines indicates the modulatory influence of biochanin-A in colon cancer treatment.
GSK‐3β↓, It blocked the “Akt and GSK3β phosphorylation and boosted the degradation of β-catenin” ( Mahmoud et al., 2017).
β-catenin/ZEB1↓,
RadioS↑, Biochanin-A when combined with gamma radiation on HT29 cells, which is resistant to radiation, had revealed a reduction in cell proliferation.
ROS↑, Raised levels of ROS, lipid peroxidation, MMP, caspase-3 have been observed more in the treatment group with significant apoptosis
Casp1↑,
MMP2↓, biochanin-A influenced the tumour invasion capacity by lowering matrix-degrading enzymes (MMP 2 and MMP 9) tested in U87MG cells
MMP9↓,
EGFR↓, Biochanin-A by lowering EGFR, p-ERK (Extracellular signal related kinases), p-AKT (Protein kinase-B), c-myc, and MT-MMP1 (Membrane type matrix metalloproteinase) activation, inhibited cell survival.
ChemoSen↑, Biochanin-A synergistically improved temozolomide anti-cancer ability in GBM
PI3K↓, Cell signalling pathways MAP kinase, PI3 kinase, mTOR, matrix metalloproteases, hypoxia-inducible factor, and VEGF were inhibited by biochanin-A, making it suitable in treating GBM
MMPs↓,
Hif1a↓,
VEGF↓,
*ROS↓, anti-diabetic mechanism of biochanin-A is by decreasing oxidative stress
*Obesity↓, strongly suggest that biochanin-A has therapeutic potential in the treatment of obesity and the prevention of cardiovascular disease
*cardioP↑,
*NRF2↑, Biochanin-A up-regulated the Nrf-2 pathway while suppressing the NF-κB cascade,
*NF-kB↓, By activating the Nrf-2 pathway and inhibiting NF-κB activation, biochanin-A may reduce obesity and its related cardiomyopathy by decreasing oxidative stress and inflammation
*Inflam↓,
*lipid-P↓, cardio-protective effects by controlling lipid peroxidation
*hepatoP↑, biochanin-A influence the elevated hepatic enzyme level, such as AST, ALP, ALT, bilirubin, etc., and found to be a promising molecule in hepatotoxicity models
*AST↓,
*ALP↓,
*Bacteria↓, The results indicate that biochanin-A may be an effective alternate to antibiotics for alleviating SARA in cattles
*neuroP↑, the neuroprotective effects of biochanin-A might be attributed to the activation of the Nrf2 pathway and suppression of the NF-κB pathway
*SOD↑, Biochanin-A reduced oxidative stress in the brain by augmenting SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase) and repressing MDA (malondialdehyde) levels.
*GPx↑,
*AChE↓, Acetylcholinesterase activity was found decreased in a dose-reliant manner amongst biochanin-A treated animals
*BACE/β-secretase↓, Biochanin-A non-competitively inhibited BACE1 with an IC 50 value of 28 μM.
*memory↑, estore learning and memory deficits in ovariectomized (OVX) rats.
*BioAv↓, The bioavailability of biochanin-A is poor.
*NRF2↑, CA and CS themselves are not electrophilic, but in response to oxidation, become electrophilic, and then activate the Keap1/Nrf2/ARE (antioxidant response element)
*GSH↑, EP3s dramatically increase GSH levels by transcriptional upregulation of the enzyme’s synthetic machinery via Nrf2 activation.
*neuroP↑, neuroprotective diterpene-type PEDs such as CA and CS
*Inflam↓, CA and CS have been reported to display beneficial effects against acute and chronic inflammation, cardiovascular diseases, obesity, and cancer [94, 95],
*cardioP↑,
*Obesity↓,
*angioG↓, antiangiogenesis [99], protection against cisplatin [100], induction of neurotrophins [101], protection in an Alzheimer’s disease model [102], inhibition of NF-κB
chemoP↑,
*NF-kB↓,
*antiOx↑, antioxidant (8), anti-inflammatory (9) and anti-obesity (10) properties.
*Inflam↓,
*Obesity↓,
chemoPv↑, Many laboratories have reported that capsaicin possesses chemopreventive and chemotherapeutic effects
Apoptosis↑, Capsaicin has been shown to induce apoptosis in many different types of cancer cell lines including pancreatic (19) colonic (24), prostatic (25), liver (26), esophagieal (27), bladder (28), skin (29), leukemia (30), lung (31), and endothelial cells (
selectivity↑,
TRPV1↑, Transient receptor potential vanilloids (TRPVs) are receptors of capsaicin which lead to Ca2+-mediated mitochondrial damage and cytochrome c release.
Ca+2↑,
mtDam↑,
Cyt‑c↑,
P53↑, Capsaicin was found to induce p53 phosphorylation at the Ser-15 residue (30) and enhanced p53 acetylation through down-regulation of sirtuin 1 (
SIRT1↓,
TumCCA↑, Capsaicin induced G0/G1 phase arrest in human esophageal carcinoma cells with an increase of p21 and a decrease of CDK4, CDK6 and cyclin E (
P21↑,
CDK4↓,
CDK6↓,
cycE/CCNE↓,
angioG↓, Capsaicin has anti-angiogenic properties both in vitro and in vivo
TumMeta↓, Capsaicin treatment significantly reduced the metastatic burden in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice (57).
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*BBB↓, crosses the blood–brain barrier, alters neurotransmitter levels, and accumulates in brain regions involved in cognition.
*GutMicro↑, capsaicin appears to undergo microbial transformation and influences gut microbial composition, favoring short-chain fatty acid producers and suppressing pro-inflammatory taxa. often favoring the growth of beneficial taxa such as Ruminococcaceae, Lac
Obesity↓, These changes contribute to anti-obesity, anti-inflammatory, and potentially anticancer effects
*Inflam↓,
*AntiCan↑,
*TRPV1↑, Capsaicin is a potent agonist perceived by TRPV1, a transmembrane cation channel that functions with Ca2+.
*Ca+2↑, causes an increase in Ca2+ flux,
*antiOx↑, Capsaicin is a bioactive compound of chili peppers responsible for their spicy flavor, which also shows antioxidant, anti-obesity, analgesic, anti-inflammatory, anticarcinogenic, and cardioprotective effects
*cardioP↑,
*BioAv↓, capsaicin exhibits low systemic bioavailability due to its rapid metabolism in the liver and other tissues, resulting in a short plasma half-life of approximately 25 min in humans
*Half-Life↓,
*BioAv↝, Capsaicin’s bioavailability is determined by multiple interrelated factors, including its physicochemical properties, metabolic transformations, route of administration, and the biological context of the host, including gut microbiota composition.
*BioAv↑, For instance, polymeric micelles, liposomes, and hydroxypropyl-β-cyclodextrin complexes have demonstrated the capacity to enhance capsaicin’s oral bioavailability, prolong its plasma half-life, and improve therapeutic consistency
*neuroP↑, capsaicin exposure alters glutamate, GABA, and serotonin levels in distinct brain regions, with potential implications for neuroprotection, mood regulation, and energy metabolism.
Apoptosis↑, apoptosis is the main mechanism by which capsaicin induces cell death in cancer cells.
p38↑, capsaicin triggers a calcium flux within the cell via TRPV1, activating the p38 pathway.
ROS↑, As a result, reactive oxygen species (ROS) are produced, along with depolarization of the mitochondrial membrane potential and opening of the mitochondrial permeability transition pore.
MMP↓,
MPT↑,
Cyt‑c↑, Consequently, cytochrome c is released, the apoptosome is assembled, and caspases are activated, ultimately leading to cell death
Casp↑,
TRIB3↑, capsaicin enhances TRIB3 gene expression, which allowed an increase in the antiproliferative and proapoptotic effects of TRIB3 in cancer cells
NADH↓, Capsaicin has also been seen to downregulate and inhibit tumor-associated NADH oxidase (tNOX) and Sirtuin1 (SIRT1) in multiple cancer cell lines such as bladder cancer, which led to reduced cell growth and migration
SIRT1↓,
TumCG↓,
TumCMig↓,
TOP1↓, pointing out that capsaicin had an inhibitory effect on topoisomerases I and II, causing a reduction in metabolic activity and proliferation of a human colon cancer cell line
TOP2↓,
β-catenin/ZEB1↓, with capsaicin, the β-catenin transcription gets downregulated
*ROS↓, Capsaicin has also been proven to alleviate redox imbalance or oxidative stress, thanks to its antioxidative activity.
*Aβ↓, Alsheimer’s disease, attenuating neurodegeneration in mice by reducing amyloid-beta levels via the promotion of non-amyloidogenic processing of amyloid precursor protein
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Obesity↓, Capsaicin can also promote weight loss, making it potentially useful for treating obesity.
Half-Life↓, The clinical usefulness of capsaicin is limited by its short half-life.
antiOx↑, Capsaicin exerts analgesic, antioxidant, cardioprotective, anticancer and thermogenic effects, and it can promote weight loss
TRPV1↑, (TRPV1), to which capsaicin binds specifically.
STAT3↓, capsaicin may inhibit signal transducer and activator of transcription 3 (STAT3), but the minimal concentration needed to inhibit STAT3 (50 M) is substantially higher than the concentration required to stimulate TRPV1 (1–5 M)
Ca+2↑, mechanisms appear to involve accumulation of intracellular Ca2+, generation of reactive oxygen species, disruption of mitochondrial membrane potential and upregulation of the transcription factors NF-κB and STATS.
ROS↑,
MMP↓,
*neuroP↑, Capsaicin has demonstrated therapeutic potential in several animal models of Alzheimer's disease (AD).
*tau↓, capsaicin substantially ameliorated synaptic damage and tau hyperphosphorylation induced by cold water stress.
*Inflam↓, capsaicin appeared to activate TRPV1 in M1/M2 dopaminergic neurons, which may alleviate neuro-inflammation and oxidative stress from activated glia
*ROS?,
*Bacteria↓, Carvacrol, either alone or in combination with other compounds, has a strong antimicrobial effect on many different strains of bacteria and fungi that are dangerous to humans
*Inflam↓, Carvacrol also exerts strong anti-inflammatory properties by preventing the peroxidation of polyunsaturated fatty acids by inducing SOD, GPx, GR, and CAT, as well as reducing the level of pro-inflammatory cytokines in the body.
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*toxicity↓, Carvacrol is considered a safe compound despite the limited amount of data on its metabolism in humans.
*Pain↓, carvacrol has been used as a substitute for cretol and carbolic acid in the treatment of toothache, sensitive dentine, and alveolar abscess, and as an antiseptic in the pulp canals of the teeth
*other↑, because it has much greater activity as a mosquito repellent than the commercial preparation, N,N-diethyl-m-methylbenzamide
*cardioP↑, other biological activities, including cardio-, reno-, and neuroprotective [20]; immune response-modulating [21]; antioxidant; anti-inflammatory [22];
*RenoP↑,
*neuroP↑,
*antiOx↑,
*AntiDiabetic↑, antidiabetic; hepatoprotective [28]; and anti-obesity properties
*hepatoP↑,
*Obesity↓,
*AntiAg↑, figure 1
*BioAv↓, challenges surrounding the wider use of carvacrol in food or feed are its unpleasant and pungent taste at higher doses; low bioavailability;
BioAv↝, sensitivity to the surrounding environment, such as in processing conditions (e.g., heat or other ingredients); and the acidic environment in the digestive tract.
*OS↑, pneumonia. Administration of carvacrol to mice (10, 25, 50 mg/kg) was associated with increased survival and significantly reduced bacterial load
MMP↓, carvacrol was found to cause greater membrane depolarization and increased oxidative stress in E. coli cells;
ROS↑,
*MDA↓, In studies conducted in guinea pigs, carvacrol concentrations of 120 and 240 μg/mL have been shown to reduce malondialdehyde levels compared to the control group
*lipid-P↓, Carvacrol prevents lipid peroxidation by inducing SOD, GPx, GR, and CAT [85,86].
*COX2/PTGS2↓, A decrease in COX-2 gene expression was found at carvacrol concentrations of 0.008% and 0.016%
*Dose↝, Phase I clinical trial, carvacrol was administered to healthy subjects at 1 and 2 mg/kg/day for 1 month, and no critical adverse reactions
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*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2/PTGS2↓,
*MDA↓,
*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
*antiOx↑, including anti-oxidant, anti-inflammatory, antilipidemic, antidiabetic, and antihypertensive activities.
*Inflam↓,
*AntiDiabetic↑,
*Obesity↓, chlorogenic acid as a nutraceutical for the prevention and treatment of metabolic syndrome and associated disorders, including in vivo studies, clinical trials, and mechanisms of action
*Wound Healing↑, It was found that chlorogenic acid accelerated wound healing.
*BP↓, Significant reductions of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were observed
*Dose↝, A total of 23 healthy subjects (four men and 19 women) were given water (control) and 400 mg of chlorogenic acid dissolved in 200 mL of low nitrate water.
*ROS↓, the mechanism proposed was that chlorogenic acid scavenges reactive oxygen species (ROS) generated by consumption of high-fat diet, which suppresses the expression of inflammation, and consequently reduces fat accumulation,
*Fas↓, chlorogenic acid supplementation in high-fat diet-induced-obese mice significantly inhibited fatty acid synthase (FAS),
*HMG-CoA↓, As for hypercholesterolemia, chlorogenic acid has been found to inhibit 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR)
*GutMicro↑, high-CGAs coffee (80.8 mg) induced a significant increase in the growth of Bifidobacterium spp. as well as Clostridium coccoides-Eubacterium rectale group, the latter group having also potential to benefit human health.
*BioAv↓, CGA’s oral bioavailability remains limited, prompting research into optimized extraction methods, novel formulations, and structural modifications.
*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, hepatoprotective, cardioprotective and neuroprotective effects, and modulation of lipid and glucose metabolism
*Inflam↓,
*Bacteria↓,
*hepatoP↑,
*cardioP↑,
*neuroP↑,
*ROS↓, CGA action include inhibition of oxidative stress, regulation of inflammatory responses through modulation of the NF-κB pathway and activation of the Nrf2 pathway
*NF-kB↓, inhibition of NF-κB
*NRF2↑,
*Obesity↓, Research demonstrates that CGA may influence body weight regulation through multiple pathways, including modulation of gut microbiota, reduction of inflammation, regulation of adipogenesis, and stimulation of thermogenesis.
*GutMicro↑, increasing the abundance of probiotic bacteria such as Bifidobacterium and Lactobacillus, while reducing the abundance of bacterial strains found in obese patients and animals, such as Desulfovibrionaceae, Ruminococcaceae, Lachnospiraceae, and Erysip
*AntiAg↑, antiplatelet effects of CGA are supported by both in vitro and in vivo studies
*cardioP↑, CGA was recognized as a compound with high cardioprotective potential, considering its antioxidant, anti-inflammatory, and antihypertensive activities
*AntiDiabetic↑, CGA alleviates the effects of type 2 diabetes mellitus (DM) and helps prevent its development
*NLRP3↓, CGA also inhibits the NLRP3 inflammasome via Nrf2 activation, significantly decreasing proteinuria, creatinine, and urea levels in diabetic rats
*OCLN↓, figure 3
*VEGF↓,
BioAv↝, CGA is water-soluble but highly unstable when exposed to elevated temperature, light, oxygen, or alkaline pH
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*Aβ↓, chlorogenic acid can reduce Aβ plaques in Alzheimer’s disease model mice by 37%, indicating its neuroprotective potential.
*neuroP↑,
*cardioP↑, Similarly, CGAs offer protection to the cardiovascular system, gastrointestinal tract, kidneys, and liver, while additionally preventing metabolic syndrome and displaying anticancer and antimicrobial capabilities.
*GastroP↑,
*RenoP↑,
*hepatoP↑,
*Obesity↓,
*Bacteria↓,
*BioAv↑, hydroxycinnamoyl-CoA quinate hydroxycinnamoyl transferase, HQT in tomatoes significantly enhances CGA accumulation without significantly altering the levels of other soluble phenolic botanical drugs.
*BioAv↑, Mechanistic studies have shown that dietary fats (such as soybean oil and coconut oil) can significantly enhance the permeability of CGA in the Caco-2 monolayer by increasing cell membrane fluidity
*BioAv↑, Following oral administration of CGA, the acidic environment in the stomach helps maintain the structural stability of CGA, with approximately one-third of the dose entering the blood system through passive diffusion in the small intestine, while the
*ROS↓, CGA pretreatment markedly diminished ROS caused by PD toxins
*GutMicro↑, CGA works with the gut microbiota and its metabolites to alleviate post-infectious irritable bowel syndrome (PI-IBS)
*IBI↑, CGA increases intestinal damage repair, decreases MCT-1 and TFF-3 expression, and suppresses NF-κB expression
*MCT1↓,
*NF-kB↓,
*DNMT1↓, Liver Cancer, DNMT1 protein expression↓
*Imm↑, Chitosan is capable to stimulate immune responses.
*BioAv↑, By attaching galactose molecules to the chitosan molecules, a new water-soluble compound, glycated chitosan (GC), was synthesized.
eff↑, GC was designed for immune stimulations in combination with phototherapies in the treatment of metastatic tumors.
*toxicity↓, No toxic effects of GC were observed in cultured cells or in animal studies. I
*TNF-α↑, immunological effect of GC was investigated through its stimulation of TNFα secretion by macrophages in vitro.
*Obesity↓, a dietary supplement for weight loss
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TumVol↓, chitosan-based nanoparticles reduced tumors (doxorubicin (DOX) + survivin siRNA and curcumin + siRNA).
toxicity↓, Their initial studies reveal low toxicity and long-term medication delivery.
Half-Life↑,
eff↑, that allows drug release in reductive cellular environments (especially cancer cells with elevated glutathione levels),
selectivity↑, This clever nanocarrier reacts to intracellular cues and delivers its therapeutic payload mostly to cancer cells while protecting healthy tissues
Dose↝, These co-delivery systems take advantage of chitosan's mucoadhesive properties and protection against enzymatic degradation, enabling oral or nasal administration routes that traditionally pose challenges for peptide delivery
*BDNF↑, Chitosan nanoparticles delivering a combination of brain-derived neurotrophic factor (BDNF) protein and Nrf2 plasmid DNA have been shown to support synaptic plasticity, inhibit oxidative stress, and slow neurodegeneration.
*NRF2↑,
*ROS↓,
*neuroP↑,
*memory↑, In preclinical trials, such strategies improved memory retention, cognitive performance, and neuronal survival in rodent models
*cognitive↑,
*Obesity↓, obese non-human primates illustrated how chitosan-based codelivery of metformin and fibroblast growth factor 21 (FGF21) plasmid DNA targeted adipose tissue to achieve a 40 % reduction in visceral fat
AGEs↓, Chitosan that can help reduce AGE (advanced glycation endproducts) levels in patients with prostate cancer.
Wound Healing↑, Chitosan is approved by the FDA for use in wound dressings
Obesity↓, been used in published clinical trials for weight loss but is not approved for the purposes of this study.
*antiOx↑, wide range of beneficial effects, including antioxidant, antimutagenic, antigenotoxic, anti-cancer, and anti-obesogenic activities.
*toxicity↓, Dietary supplements containing chlorophyll and chlorophyllin are available and generally considered safe, with no reported adverse side effects over several decades of human use
*BioAv↓, Due to the poor bioavailability and stability of chlorophylls, studies on chlorophylls are scarce until now.
*BioAv↑, Semi-synthetic sodium copper-chlorophyllins (SCC) . modifications enhance the stability, solubility in water, and accessibility of SCC
*neuroP↑, figure 3
*Obesity↓,
*AntiCan↑, rats subjected to dietary heme, which mimics red meat ingestion, demonstrated that natural chlorophylls inhibit colonic cytotoxicity, proliferation of colonic epithelial cells, epithelial cell turnover, and the formation of lipid radicals induced by
*TumCP↓, SCC has been reported to decrease the proliferation of human pancreatic cancer cell lines in vitro
*PhotoS↑, Chlorophyll acts as a photosensitizer due to its natural ability to absorb light.
*neuroP↑, chlorophyll may exert its neuroprotective effects is through its antioxidant properties. Oxidative stress
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*toxicity↓, Unlike what happens in other mammals -pets- included, theobromine is safe for humans and has fewer unwanted effects than caffeine
*eff↑, Theobromine, which is found in higher amounts than caffeine, seems to be behind several effects attributed to cocoa intake.
*Half-Life↑, Half-life of theobromine is higher than caffeine even in rodents, which have a faster hepatic metabolism. The mean half-life in plasma from healthy volunteers is approximately 10 h
*eff↑, Theobromine is useful in asthma and in other respiratory tract problems such as cough for which no definitive drug has been developed.
*Inflam↓, Benefits of the theobromine on cough seem to be related with its anti-inflammatory potential as well as with modulation of airway reactivity
*HDL↑, The results of the clinical trial NCT01481389 (clinicaltrials.org) suggest that theobromine but not flavonoids is the responsible for the increase in HDL levels in individuals taking cocoa products
*Obesity↓, theobromine has been considered useful for weight loss and it is supplemented to herbal tea preparations
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*lipid-P↓, inhibition of lipid peroxidation and the protection of LDL-cholesterol against oxidation, and increase resistance to oxidative stress.
*ROS↓,
*Inflam↓, decreasing platelet function and inflammation along with diastolic and systolic arterial pressures, which, taken together, may reduce the risk of cardiovascular mortality.
*BP↓,
*cardioP↑, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*chemoPv↑, They also have antiproliferative, antimutagenic, and chemoprotective effects, in addition to their anticariogenic effects.
*BioAv⇅, great controversy surrounding the bioavailability of phenolics in general and of cocoa derivatives in particular.
*antiOx↑, Cocoa has more phenolics and higher antioxidant capacity than green tea, black tea, or red wine
*Risk↓, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*5LO↓, cocoa polyphenols decrease the plasma concentration of proinflammatory cysteinyl leukotrienes through inhibition of 5-LOX, as demonstrated by Sies et al.
*AntiAg↑, Moreover, cocoa decreases not only platelet aggregation, but also adhesion. 234 mg cocoa phenolics a day for 28 days
*Imm↑, Kenny et al. [21] demonstrated that cocoa oligomers are potent stimulators of both the innate immune system and early events in adaptive immunity.
*NF-kB↓, nd their dimeric forms were found to inhibit the NF-κB activation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in T cells,
*other↓, in vivo and in vitro models have provided evidence that pure polyphenols and natural polyphenol plant extracts can modulate intestinal inflammation.
CYP1A1↓, polyphenol cocoa extract leads to the induction of CYP1A1 in breast cancer cells.
COX2/PTGS2↓, hey also inhibited the expression of COX-2,
*Obesity↓, Ferrazzano et al. hypothesized that the polyphenols contained in cocoa may have antiobesity effects due to their ability to suppress fatty acid synthesis while stimulating cell energy expenditure in the mitochondria
*cognitive↑, Moreover, cocoa consumption may also have beneficial effects on satiety, cognitive function, and mood [93].
*antiOx↑, Chicoric acid (CA), a natural phenolic acid extracted from chicory and the echinacea (purple coneflower) plant (Echinacea purpurea), has been regarded as a nutraceutical that has powerful antioxidant and antiobesity activities.
*Obesity↓,
*memory↑, CA prevented LPS-induced memory impairment and neuronal loss through behavioral tests and histological examination.
*Aβ↓, CA prevented LPS-induced increases in amyloid β (1-42 specific) (Aβ1-42) accumulation,
*MAPK↓, CA down-regulated LPS-induced glial overactivation by inhibiting the MAPK and NF-κB pathway.
*NF-kB↓,
*iNOS↓, CA reduced the levels of NF-κB transcriptionally regulated inflammatory mediators and cytokines such as iNOS, cyclooxygenase-2 (COX-2), IL-1β, and TNF-α in both mouse brain and BV2 microglial cells.
*COX2/PTGS2↓,
*IL1β↓,
*TNF-α↓,
*NF-kB↓, Chicoric acid supplementation prevents systemic inflammation-induced memory impairment and amyloidogenesis via inhibition of NF-κB.
*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.
*Bacteria↓, multiple pharmacological properties such as antibacterial, antifungal, antiparasitic, antineuraminidase, antioxidant, anti-inflammatory, and anticancer activities.
*AntiFungal↑,
*antiOx↑,
*Inflam↓,
AntiCan↑,
*AntiDiabetic↑, also demonstrated an antidiabetic effect, through its role in the prevention of obesity and metabolic problems associated with high-fat diets
*Obesity↓,
TumCCA↑, Anticancer mechanisms of carvone are due to its different actions against checkpoints of cancer cells such as inducing apoptosis and cell cycle arrest
*AntiArt↑, figure 2
Imm↑,
*P450↓, decreased levels of phase I enzymes (cytochrome P450 and cytochrome b5) with increased levels of phase II enzymes (GR, GST, and GSH) and increased expression of Bax, caspase-3, and caspase-9 with decreased expression of mutated p53 and Bcl-2 in anima
*GSR↑,
GSTs↑,
GSH↑,
BAX↑,
Casp3↑,
TumCP↓, Results showed that L-carvone exhibited a strong antiproliferative effect against MCF7 (IC50 = 1.2 mM) and MDA MB 231 cells (IC50 = 1.0 mM), inhibited the migration of breast cancer cell lines, and induced apoptosis.
TumCMig↓,
Apoptosis↑,
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*AntiCan↑, gained increasing interest due to its proposed anti-cancer, anti-obesity, anti-inflammatory, antioxidant, and lipid-lowering effects, in addition to its thermogenic capacity.
*Obesity↓,
*Inflam↓,
*lipid-P↓,
*BioAv↓, intact curcumin in the body may be too low (<1 microM) and not sufficient to affect signaling and gene expression, as observed in vitro with cultured cells (10–20 microM).
*BioAv↑, a myriad of nanoformulations have been developed that either lead to a systemic increase in curcumin or are targeted to specific cells, tissues, or organelles
*BioAv↑, latest generation of curcumin nanoformulations can increase the bioavailability of free curcumin in plasma greater than 100-fold and have superior absorption, cellular uptake, BBB permeability, and tissue distribution
*BioAv↑, In a clinical study, the authors found that 2 g of curcumin administered concomitantly with 20 mg of piperine, an inhibitor of hepatic and intestinal glucuronidation, appeared to promote a significant 2000% increase in the oral bioavailability of cur
*BioAv↑, rats in which piperine pre-administration was performed before receiving curcumin, there was a significant increase in the oral bioavailability of curcumin, especially at 6 h after piperine administration
*BioAv↑, Nanotechnology-based delivery systems such as micelles, liposomes, and polymeric, metal, and solid lipid nanoparticles have also been applied to enhance curcumin bioavailability
*ROS↓, Curcumin was effective against ischemia/reperfusion (I/R) lesions, as well in various experimental models, primarily through antioxidant actions such as scavenging ROSs [153], increasing mitochondrial superoxide dismutase (SOD) activity and decreasin
*mt-SOD↑,
*MDA↓,
*BBB↓, Curcumin has poor bioavailability, especially in the brain, where the BBB further limits its absorption
*Aβ↓, curcumin appears to reduce the production of Aβ also by affecting a second enzyme required for the cleavage of APP
*GSK‐3β↓, the inhibition of GSK3β by curcumin would hinder both Aβ production and tau aggregation
*tau↓,
*neuroG↑, prolonged treatment of aged rats with curcumin stimulates neurogenesis in the hippocampus
*memory↑, chronic curcumin administration improved memory acquisition and consolidation in both adult and aged rats
cardioP↑, curcumin has been investigated to promote cardioprotective effects against chemotherapy-induced cardiotoxicity
*other↝, The most common fermented foods and beverages require lactic acid bacteria (LAB), AAB, bacilli or other bacteria, yeasts, or filamentous fungi.
*toxicity↓, Fermented foods that contain appreciable levels of fermentation-produced organic acids (>100 mM), combined with low water activity, salt, nitrite and other antimicrobials, have a long record of food safety78. Likewise, beverages containing 4% or more
*toxicity↓, Food fermentations can also enhance food safety and nutritional quality by removing toxic or anti-nutritive compounds from the raw ingredients.
*Obesity↓, Yoghurt consumption is associated with reductions in adiposity factors (BMI, waist circumference)105, type 2 diabetes mellitus and cardiovascular disease
*AntiDiabetic↑,
*cardioP↑,
*GutMicro↑, including nutritive alteration of raw ingredients and the biosynthesis of bioactive compounds, modification of the human gut microbiota, and development and modification of the immune system
*Imm↑, As approximately 70% of the human immune system is located in the gastrointestinal tract
*GutMicro↑, Alternatively, the high-fermented food diet steadily increased microbiota diversity and decreased inflammatory markers.
*Inflam↓, Fermented food intake decreases markers of host inflammation
*Imm↑, The data highlight how coupling dietary interventions to deep and longitudinal immune and microbiome profiling can provide individualized and population-wide insight.
*Obesity↓, Large cohort studies as well as limited interventional studies have linked the consumption of fermented foods with weight maintenance and decreased diabetes, cancer, and cardiovascular disease risks
*AntiDiabetic↑,
*AntiCan↑,
*cardioP↑,
*IL6↓, inflammatory serum proteins that decreased over the fermented food intervention including IL-6, IL-10, and IL-12b
*IL10↓,
*IL12↓,
Risk↓, Prospective cohort studies linked higher kimchi intake with a lower incidence of cancer and metabolic syndrome and an increased likelihood of achieving normal body weight.
*Obesity↓,
*GutMicro↑, Improving the gut microbiome and reducing inflammation through dietary inputs like fermented foods may therefore be a path to improving human health status
*Inflam↓,
*BP↓, figure 2
*LDL↓,
*HDL↑,
*CRP↓,
*IL6↓,
*TNF-α↓,
*Obesity↓,
*AntiDiabetic↑,
*cardioP↑, fermented dairy consumption was associated with a decreased risk of general CVD compared with controls
*GutMicro↑, yogurt consumption also coincided with transient increases in Streptococcus thermophilus and Bifidobacterium animalis subsp. lactis in feces, microbes commonly found in yogurt cultures, suggesting a role for the gut microbiome in mediating effects [
*neuroP↑, Evidence also suggests a potential protective role of fermented foods against age-related neurologic diseases such as dementia and Alzheimer’s disease.
*cognitive↑, 30 participants with Alzheimer’s disease found that daily consumption of 200 mL milk fermented with L. acidophilus, Lacticaseibacillus casei, B. bifidum, and Limosilactobacillus fermentum (2 × 109 CFU/g each) for 12 wk improved mini-mental state exam
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*antiOx↑, spanning antioxidant, anti-inflammatory, antitumor, antidiabetic, neuroprotective, and gastroprotective domains.
AntiTum↑,
*AntiDiabetic↑,
*neuroP↑, The neuroprotective potential of limonene has been demonstrated in different neurodegenerative diseases (NDs), including multiple sclerosis, stroke, epilepsy, Alzheimer’s disease (AD), and anxiety
*GastroP↑,
*ROS↓, we explore its molecular mechanisms, ranging from reactive oxygen species mitigation
*toxicity↓, Its low toxicity and high bioavailability support its potential as a safe adjunct or alternative in phytotherapy.
*BioAv↑,
ChemoSen↑, combining limonene with tamoxifen increases the anticancer efficacy by inducing apoptosis in MCF 7 BC cells
BAX↑, MCF-7 cells, D-limonene treatment significantly increases the expression of Bcl-2-associated X protein (Bax) and p53 while downregulating Bcl-2, inducible nitric oxide synthase (iNOS), and COX-2
P53↓,
Bcl-2↓,
iNOS↓,
COX2/PTGS2↓,
eff↑, IC50 of free limonene was reported to be 985.00 μg/mL, whereas its encapsulation in chitosan nanoparticles (LimChiNPs) significantly reduced the IC50 to 650.70 μg/mL.
ROS↑, Furthermore, this dual therapy augmented intracellular reactive oxygen species production and promoted cell cycle arrest predominantly at the G1 phase via the modulation of cyclin D1 and B1 [20].
TumCCA↑,
cycD1/CCND1↓,
CycB/CCNB1↓,
TumCMig↓, migration capacity of MCF-7 cells was also markedly inhibited under the combined regimen, suggesting potential to curb metastatic progression
*lipid-P↓, Limonene therapy resulted in a decrease in lipid peroxidation levels and an increase in the level of glutathione, a major antioxidant that helps protect cells from damage
*GSH↑,
*SOD↑, Moreover, the activity of antioxidant enzymes (SOD and glutathione peroxidase (GPx)) was improved, indicating that the body’s natural defense system was functioning better again
*GPx↑,
*hepatoP↑, limonene treatment has been shown to mitigate liver damage caused by DEN/2-AAF exposure by reinforcing the antioxidant defenses in hepatic cells
*glucose↓, D-limonene consistently lowered fasting glucose and HbA1c, improved lipid profiles, and enhanced antioxidant defenses (e.g., increased SOD, CAT, and GSH levels)
*AGEs↓, D-limonene has been shown to inhibit the formation of advanced glycation end products (AGEs) through multiple mechanisms,
*Obesity↓, Notably, limonene also stimulates differentiation and glucose uptake in adipocytes, suggesting a role in counteracting insulin resistance and obesity-related metabolic dysfunction
*Aβ↓, The neuroprotective properties of limonene find expression in suppressing Aβ-induced cell death and decreasing ROS levels
*AChE↓, Further insights into the molecular mechanism of limonene’s inhibition of AChE have been provided by molecular dynamics simulations
*diuretic↑, These properties are diuretic, hepatoprotective, anticolitis, immunoprotective, antiviral, antifungal, antibacterial, antiarthritic, antidiabetic, antiobesity, antioxidant and anticancer effects
*hepatoP↑,
*Imm↑,
*Bacteria↓,
*AntiArt↑,
*AntiDiabetic↑,
*Obesity↓,
*antiOx↓,
*AntiCan↑,
Dose?, The main phytochemicals are: carotenoids; flavonoids (e.g., quercetin, chrysoeriol, luteolin-7-glucoside); phenolic acids (e.g., caffeic acid, chlorogenic acid, chicoric acid); polysaccharides (e.g., inulin); sesquiterpene lactones (e.g., taraxinic a
*antiOx↑, bioactivities of EGCG, including its antioxidant, anti-inflammatory, anticancer, cardiovascular protective, metabolic regulatory, neuroprotective, gut microbiota-modulating, and antimicrobial properties.
*Inflam↓,
*AntiCan↑,
*cardioP↑,
*neuroP↑,
*GutMicro↑,
*AntiBio↑,
*ROS↓, Figure 1, anti inflammatory
*TNF-α↓,
*IL6↓,
TumCP↓,
*LDL↓, cardioprotective
*NO↓,
*Obesity↓, Metabolic syndrome
*p‑tau↓, nervous system
*Aβ↓,
*NRF2↑, , EGCG has been shown to activate the Keap1/P62/Nrf2 signaling pathway,
*SOD↑, upregulation of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, indirectly diminishing the levels of intracellular oxygen free radicals
*Catalase↑,
*GPx↑,
*NLRP3↓, EGCG also restores autophagy levels, suppresses the activation of the NLRP3 inflammasome by inhibiting the mammalian target of rapamycin signaling pathway
*mTOR↓,
TumCCA↑, Cancer: induce cell cycle arrest and inhibit tumor cell proliferation
NRF2↓, EGCG inhibits CCL5-stimulated lung cancer cell proliferation by down-regulating Nrf2 expression
Apoptosis↑, Inducing Apoptosis in Cancer Cells
SIRT1↓, EGCG activates the mitochondrial apoptotic pathway by downregulating SIRT1 expression to modulate the SIRT1-p53 axis
miR-25-5p↓, In breast cancer, EGCG induces apoptosis by inhibiting miR-25 expression and elevating PARP, pre-caspase-3 and pre-caspase-9 protein levels
PARP↑,
Casp3↑,
Casp9↑,
ER Stress↑, in multiple myeloma, EGCG promotes apoptosis by activating the endoplasmic reticulum stress pathway
TumAuto↑, EGCG induces autophagic cell death in breast cancer cells by retaining YAP1 in the cytoplasm and promoting the assembly of the CHMP2B-VPS4B complex
EMT↓, EGCG has been demonstrated to inhibit EMT, invasion, and migration by blocking the TGFβ/Smad signaling pathway
TumCI↓,
TumCMig↓,
TGF-β↓,
Smad1↓,
STAT3↓, EGCG can directly bind to STAT3, reducing nuclear localization and inhibiting the transcription of PLXNC1.
VEGF↓, widely believed that EGCG can block this process by reducing the expression of vascular endothelial growth factor, a key factor in angiogenesis,
angioG↓, The inhibition of angiogenic mimicry by EGCG through the Twist/VE-calmodulin/AKT pathway has also been demonstrated in prostate cancer cells
Imm↑, Acting as an Immunomodulator
EGFR↓, EGCG possesses the ability to interact with EGFR and inhibit activity, strengthening the anticancer evidence for EGCG
*GutMicro↑, EGCG can regulate the balance of gut flora. For example, EGCG can inhibit the growth of harmful bacteria such as Escherichia coli and Salmonella, while promoting the proliferation of probiotics like Bifidobacterium and Lactobacillus
*Bacteria↓, Antibacterial and Antiviral Properties of EGCG
*AntiViral↑,
*BioAv↓, EGCG, its low bioavailability in the human body limits clinical efficacy.
*BioAv↑, Nanotechnology strategy of EGCG.
*eff↑, Co-encapsulation assay of EGCG with quercetin shows that the two synergistically enhanced the antioxidant capacity of EGCG
*BioAv↑, Combining EGCG with resveratrol increases its solubility and significantly improves its absorption in the small intestine.
eff↑, combination of EGCG and curcumin inhibits the activity of metabolic enzymes, reduces the rate of metabolism in the liver and enhances its antitumor efficacy
ChemoSen↑, synergistic effects of EGCG combined with chemotherapeutic agents such as 5-fluorouracil, celecoxib, cisplatin, and tamoxifen have also been reported
*toxicity↝, The European Food Safety Authority notes in scientific opinion that daily oral doses of 800 mg or higher of EGCG represent a common starting point for observed cases of liver injury
*Inflam↓, Emodin has a variety of pharmacological effects, including anti-inflammatory, anti-tumor, antibacterial, immune enhancement, lipid-lowering, blood glucose-lowering, kidney protection, etc.
*AntiTum↑,
*Bacteria↓,
*Imm↑,
*glucose↓,
*RenoP↑,
*TLR4↓, i.p 40 mg/kg Inactivating the TLR4/MyD88/NF-κB/NLRP3 pathway
*MyD88↓,
*NLRP3↓,
*NF-kB↓, 20 μM Inhibiting ROS-mediated NF-κB activation
*PI3K↓, Inhibiting the PI3K/mTOR/GSK3β signaling pathway
*mTOR↓,
*GSK‐3β↓,
*Hif1a↓, LPS-induced acute lung injury (ALI) in rats oral 20 mg/kg, 40 mg/kg Inhibiting the mTOR/HIF-1α/VEGF signaling pathway
*VEGF↓,
*GutMicro↑, oral 8.75, 17.5 and 35 mg/kg Increasing the abundance of beneficial intestinal microbiota and inhibiting the abundance of harmful bacteria
*Obesity↓, Similarly, in high-fat diet-induced obese mice, treatment with emodin (80 mg/kg) reduced body weight
*AntiDiabetic↑, emodin also has a good therapeutic effect on diabetic neuropathic pain (DNP), diabetic cardiomyopathy (DCM), and diabetic gastroenteropathy.
*AMPK↑, Emodin upregulates AMPK phosphorylation, downregulates mTOR phosphorylation, and reduces the expression of Bcl-2-associated X protein (Bax) and cysteine-dependent aspartate-specific proteases-3 (caspase-3), indicating that emodin actively regulates a
*PPARγ↑, Most current research results indicate that emodin has the effect of activating PPARγ in a dose-dependent manner
*PPARγ↓, however, the research results of Yang et al. showed that emodin can reduce the expression of PPARγ and enhance the expression of Runx2 and OSX, thereby enhancing the differentiation into osteoblasts
*toxicity↝, Although emodin has shown hepatoprotective effects in many studies, Zheng et al. showed hepatotoxicity when a large concentration of emodin (160 μM) was administered to L02 cells,
*hepatoP↑, whereas hepatoprotective effects were observed when emodin concentrations were controlled at 10–80 μM
*AST↓, the liver function test results showed that emodin at doses of 40 mg/kg and 80 mg/kg had a better effect on reducing AST and ALT than 160 mg/kg
*ALAT↓,
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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;
*toxicity↓, Promisingly, toxicity studies have shown that GA scarcely has obvious toxicity or side effects in a variety of animal experiments and clinical trials.
*Inflam↓, anti-inflammatory mechanisms of GA mainly involved MAPK and NF-κB signaling pathways.
*NF-kB↓,
AntiTum↑, GA also has several evident pharmacological effects including anti-tumor, anti-bacterial, anti-diabetes, anti-obesity, anti-microbial and anti-myocardial ischemia
Bacteria↓,
*AntiDiabetic↑,
*Obesity↓,
*AntiBio↑,
*Stroke↓,
*NO↓, GA could inhibit the secretion of pro-inflammatory mediators nitrite, NO, PGE2 and IL-6 in a dose-dependent manner
*PGE2↓,
*IL6↓,
*MAPK↓, GA inhibits the activities of NF-κB and MAPK, subsequently inhibiting the release of inflammatory factors (TNF-α, IL-1β/6), chemokines (CCL-2, ICAM-1, TIMP-1)
*TNF-α↓,
*IL1β↓,
*MCP1/CCL2↓,
*ICAM-1↓,
*TIMP1↓,
*Obesity↓, Garcinol inhibits fat metabolism-related proteins and genes, reduces appetite, and enhances metabolism.
*Appetite↓,
*GutMicro↑, Garcinol improve lipid profiles and gut microbiota and may reduce obesity-related diseases like atherosclerosis.
BioAv↝, Garcinol shows promising oral absorption and systemic exposure in animal studies, indicating potential for clinical use.
*antiOx↑, Ginkgolide and bilobalide, which are G. biloba leaf extracts, offer diverse pharmaceutical benefits, including antioxidant, anti-inflammatory, and neuroprotective properties.
*Inflam↓,
*neuroP↑,
*ROS↓, Additionally, their effectiveness in countering oxidative stress and inflammation highlights their potential to prevent cardiovascular ailments.
*cardioP↑,
*Obesity↓, This study also suggests that these compounds have a promising impact on lipid metabolism, suggesting their significance in addressing obesity-related metabolic disorders.
*BioAv↓, Despite the low solubility and poor bioavailability, several studies have investigated the diverse physiological functions of ginkgolide A, such as its neuroprotective, hepatoprotective, anti-inflammation, and antioxidant effects
*lipidLev↓, Recent research has demonstrated the lipid-lowering, antioxidant, and anti-inflammatory properties of geraniol as well as its ability to improve endothelial function and reduce oxidative stress in preclinical animals.
*antiOx↓,
Inflam↓,
*ROS↓,
*BioAv↑, The paper delves into the various nanoformulations, including liposomes, nanoparticles, and nanoemulsions, which enhance geraniol's therapeutic efficacy and bioavailability, making it a viable option for managing metabolic syndrome.
*AntiDiabetic↑, which makes it a compelling option for the treatment of conditions such as neuroinflammation, diabetes, and obesity.
*Obesity↓,
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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.
*Inflam↓, H2 demonstrates numerous biologically therapeutic properties, including anti-inflammatory, antioxidant, anti-cancer, anti-stress, anti-apoptotic, anti-allergic effects, signaling molecule functions, regulation of redox balance
*antiOx↓,
*Stress↓,
*Dose↝, The administration methods of hydrogen include inhalation, hydrogen-rich water, hydrogen-rich saline, hydrogen-rich eye drops, and hydrogen-rich bathing.
*cardioP↑, graphical abstract and figure 4
*GastroP↑,
*BBB↑, H2 is its ability to easily cross the blood-brain barrier and penetrate biomembranes, diffusing throughout the different tissues and organs.
*eff↑, The above-cited properties led some researchers to refer to it as a "miracle" molecule
*toxicity↓, Regarding the biosafety of hydrogen, numerous reports, including those from the US government and the EU, have indicated that hydrogen is safe for biological systems, showing no acute or chronic toxicity under normal pressure
*Dose↝, human large intestine often produces approximately 70–140 mL of hydrogen daily through the action of coliform bacteria such as Escherichia coli under typical environmental conditions.
*hepatoP↑, including cardioprotective properties, improved liver function, reduced oxidative stress, and prevention of Parkinson's disease
*ROS↓,
*SOD↑, 1.5–2.0 L/day drinking HRW orally 0.55–0.65 mM 1.65–2.6 mg H2/day 8 weeks SOD: ↑ TRABS: ↓ HDL: ↑
*TBARS↓,
*HDL↑,
*LDL↓, figure 4
*Obesity↓, figure 5 obesity
*GSH↑, HRW treatment partially alleviated colitis symptoms, improved histopathological changes, significantly increased glutathione (GSH) concentration, and reduced the level of TNF-α.
*TNF-α↓,
*GutMicro↑, HRW was found to exhibit partial relief of inflammation, oxidative stress, and dysbiosis in the intestinal flora of mice with chronic ulcerative colitis (UC) induced by dextran sulfate sodium (DSS)
*DNAdam↓, HRW-treated mice exhibited decreased levels of markers associated with oxidative DNA damage, such as phosphorylated histone H2AX and 8-hydroxy-2′-deoxyguanosine, as well as markers indicative of aging
*γH2AX↓,
*p‑p38↓, Treatment with HRS also inhibited the activation of p-p38 and NF-κB while suppressing the production of several pro-inflammatory mediators,
*NF-kB↓,
*Insulin↝, d-Chiro-inositol acts through a variety of mechanisms, acting as an insulin sensitizer, inhibiting the transcription of aromatase, in addition to modulating white adipose tissue/brown adipose tissue transdifferentiation.
*CYP19↓,
*Dose↝, Unlike myo-Ins, which is readily available through the diet, primarily in corns, beans, fruits, and nuts [8], it is near impossible to consume sufficient d-chiro-Ins as only a few foods (e.g., buck wheat, soy-lecithin, carob, and lentils) contain sig
*Dose↝, Therefore, d-chiro-Ins is mainly synthesized in the body from myo-Ins
*other↝, ratio between myo-Ins and d-chiro-Ins:. In the plasma, the ratio is 40:1, while in energy-dependent tissues, such as fat or liver, this drops to 2:1. tissue types that have a highglucose consumption rate, such as the brain, display a ratio of 200:1
*Insulin↓, The combined actions of the above mechanisms result in a reduced insulin requirement, thus decreasing systemic insulin levels
*IRes↓, inositol supplementation has shown great success in counteracting IR in a variety of conditions
*Obesity↓, reported a significant reduction in BMI in patients under 30 years of age and PCOS women, suggesting that inositol may have potential as an adjunct therapy to obesity care
*BioAv↝, In a minority of patients, myo-Ins has been observed to have poor bioavailability and efficacy, leading to the phenomenon of “inositol resistance,” which is associated with patients who are unresponsive to myo-Ins supplementation.
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*antiOx↑, anti-oxidant, anti-cancer, anti-inflammatory, anti-hyperalgesic, and neuroprotective effects.
*AntiCan↑,
*Inflam↓,
*neuroP↑,
*AChE↓, Anti-Alzheimer's disease Vitexin/isovitexin In vitro ChE enzyme assay Vitexin: IC 50 = 12.16 ± 3.58 (AChE) IC 50 = 6.73 ± 0.08 (BChE) IC 50 = 51.07 ± 3.31(BACE1) Isovitexin: IC 50 = 6.24 ± 1.15 (AChE) IC 50 = 6.48 ± 0.43 (BChE) IC 50 ≥ 100 (BA
*BChE↓,
*BACE/β-secretase↓,
*Stroke↓, Data showed that vitexin exhibits protective effect against cardiac ischemia/reperfusion (I/R) injury through inhibiting the I/R-induced decrease in coronary flow
*AntiAg↓, Vitexin-containing lime leaf significantly inhibited platelet aggregation in a concentration-dependent manner
*AntiDiabetic↑, Administered orally, vitexin and isovitexin significantly reduced postprandial blood glucose both in sucrose loaded normoglycemic mice and sucrose induced diabetic rat
*AGEs↓, vitexin and isovitexin, as AGE inhibitors,
*IL1β↓, inhibition in the pro-inflammatory cytokines such as IL-1β, IL6, IL-8, TNF-α,
*IL6↓,
*IL8↓,
*TNF-α↓,
*Obesity↓, Protective effects against obesity
*BioAv↝, Unusually, vitexin and isovitexin are poorly absorbed in the gastrointestinal tract [61]. They directly reached the colon where they were hydrolysed by the gut microflora through deglycosylation and ringopening of the heterocyclic C ring
*BioAv↓, oral bioavailability of vitexin was much low (approximately 5%
*BioEnh↑, Firstly, the pre-emulsification of an oil with vegetable lecithin has been shown to increase the systemic bioavailability of certain fatty acids, without increasing total plasma lipid concentrations.
*antiOx↑, different lecithin from various sources (soy, rapeseed) or with differing PL compositions have been reported to exert varying antioxidant properties
*BioEnh↑, ported higher plasma alpha-linolenic acid (ALA) concentrations in the PL-emulsified group
*LDL↓, oybean PL in patients with primary hyperlipidemia has been reported to significantly reduce blood cholesterol levels
*HDL∅, while maintaining plasmatic HDL levels
*Obesity↓, potential of lecithin on the prevention and amelioration of obesity-related metabolic disorders
eff↑, lecithin derived from olive oil compared to that of other seed oils (sunflower, corn or soybean) as a platelet aggregation factor (PAF) antagonist
GutMicro↝, importance of gut microbiota on lipid metabolism and metabolic health renders obligatory that further research on the effect of vegetable lecithin on TMAO production and gut microbiota in general be explored.
*AntiBio↑, this compound also exhibits antimicrobial, antioxidant, anticarcinogenesis, anti-inflammatory, and antispasmodic activities, as well as a potential as a growth enhancer and immunomodulator.
*Inflam↓,
*Imm↑,
*other↝, Thymol, usually combined with glycerin, alcohol, and other volatiles, is used to make mouthwashes.
*Half-Life↝, Peak plasma concentrations (93.1 ng/ml) were reached after above 2 hr, and the mean terminal elimination half‐life was 10.2 hr.
*Obesity↓, This compound prevented obesity through several mechanisms, such as the attenuation of visceral fat
accumulation,
*GutMicro↑, as well as modulate gut microbiota
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*antiOx↑, shown to possess various pharmacological properties including antioxidant, free radical scavenging, anti-inflammatory, analgesic, antispasmodic, antibacterial, antifungal, antiseptic and antitumor activities.
*ROS↓,
*Inflam↓,
*Bacteria↓,
AntiTum↑,
IronCh↑, chelation of metal ions
*HDL↑, antihyperlipidemic (via increasing the levels of high density lipoprotein cholesterol and decreasing the levels of low density lipoprotein cholesterol
*LDL↓,
*BioAv↝, videnced the presence of thymol in the stomach, intestine, and urine after its oral administration with sesame oil at a dose around 500 mg in rats and 1–3 g in rabbits.
*Half-Life↝, Oral administration of a single dose of thymol (50 mg/kg) was rapidly absorbed and slowly eliminated approximately within 24 h.The maximum concentration (Tmax) was reached after 30 min, while approximately 0.3 h was needed for the half-life
*BioAv↑, The rapid absorption of thymol indicates that it’s mainly absorbed in the upper component of the gut
*SOD↑, scavenging of free radicals by increasing the activities of several endogenous antioxidant enzymes levels viz. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST)
*GPx↑,
*GSTs↑,
*eff↑, Thymol (0.02–0.20%) showed better antioxidant capacity than its isomer carvacrol in lipid systems due to its greater steric hindrance
radioP↑, Owing to its potent antioxidant potential, thymol showed radioprotective and anticlastogenic potential in gamma radiation induced Swiss albino mice
*MDA↓, Thymol supplementation increased the antioxidant status and decreased malondialdehyde (MDA) levels in broiler chickens
*other↑, Dietary supplementation with the combination of carvacrol–thymol (1:1) (100 mg/kg) reduced the occurrence of oxidative stress and the impairment of the intestinal barrier in weaning piglets by its potent antioxidant property
*COX1↓, by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM.
*COX2/PTGS2↓,
*AntiAg↑, Thymol (1.1 μg/ml) exhibited inhibitory effects against arachidonic-acid-induced blood coagulation and platelet aggregation in vitro
*RNS↓, Thymol inhibited ROS (IC50= 3 μg/ml), reactive nitrogen species (RNS) (IC50= 4.7) and significantly reduced generation of NO and H2O2 as well as activities of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide reduced oxidase (NADH oxi
*NO↓,
*H2O2↓,
*NOS2↓,
*NADH↓,
*Imm↑, Thymol (25–200 mg/kg) was shown to modulate the immune system in cyclosporine-A treated Swiss albino mice by enhancing the expressions of cluster of differentiation 4 (CD4),
Apoptosis↑, anticancer actions of thymol include induction of apoptosis, anti-proliferation, inhibition of angiogenesis and migration
TumCP↓,
angioG↓,
TumCMig↓,
Ca+2↑, Intracellular Ca2+ overload
TumCCA↑, Cytotoxicity by stimulating cell cycle arrest in G0/G1 phase
DNAdam↑, DNA fragmentation, Bax protein expression, activation of caspase -9, -8 and -3 & concomitant PARP cleavage, AIF translocation
BAX↑,
Casp9↑,
Casp8↑,
Casp3↑,
cl‑PARP↑,
AIF↑,
i-ROS↑, intracellular ROS, depolarizing MMP, cytochrome-c release, cleavage of caspases, DNA fragmentation, activation of apaf-1,
MMP↓,
Cyt‑c↑,
APAF1↑,
Ca+2↑, In human glioblastoma cells, thymol (200–600 μM) produced a rise in (Ca2+)i levels
MMP9↓, diminished matrix metallopeptidase-9 (MMP9) and matrix metallopeptidase-2 (MMP2) production as well as protein kinase Cα (PKCα) and extracellular signal-regulated kinases (ERK1/2) phosphorylation
MMP2↓,
PKCδ↓,
ERK↓,
H2O2↑, Thymol increased the production of ROS and mitochondrial H2O2 thereby depolarizing mitochondrial membrane potential.
BAX↑, up-regulating Bcl-2 associated X protein (Bax) expression and down-regulating B-cell lymphoma (Bcl-2)
Bcl-2↓,
DNAdam↑, Thymol (IC50= 497 and 266 mM) was shown to induce DNA damage by increasing the levels of lipid peroxidation products;
lipid-P↑,
ChemoSen↑, This study recommended the combination of thymol with various chemotherapeutic agents to minimize its toxicity on normal cells and to improve the effectiveness of cancer treatment
chemoP↑,
*cardioP↑, significant increase in the activities of heart mitochondrial antioxidants (SOD, catalase, GPx, GSH)
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*BP↓, Thymol (1, 3, and 10 mg/kg) administration decreased the blood pressure and heart rate of Wistar rats whereas thymol (5 mg/kg) attenuated blood pressure in rabbits
*AntiDiabetic↑, protective effects of thymol in metabolic disorders such as diabetes mellitus and obesity
*Obesity↓,
RenoP↑, Thymol (20 mg/kg) was shown to inhibit cisplatin-induced renal injury by attenuating oxidative stress, inflammation and apoptosis in male adult Swiss Albino rats
*GastroP↑, This gastroprotective effect of thymol is believed to be due to increased mucus secretion
hepatoP↑, Thymol (150 mg/kg) showed to inhibit paracetamol induced hepatotoxicity in mice by preventing the alterations in the activities of hepatic marker enzymes
*AChE↓, Thymol (EC50= 0.74 mg/mL) was shown to possess acetylcholine esterase inhibitory activity but much less than its isomer carvacrol
*cognitive↑, Thymol (0.5–2 mg/kg) has been shown to inhibit cognitive impairments caused by increased Aβ levels or cholinergic hypofunction in Aβ
*BChE↓, whereas thymol (100 and 1000 μg/ml) also inhibited both AChE and butyrylcholinesterase (BChE) in a dose dependent manner
*other↓, Thymol (100 mg/kg) was shown to inhibit collagen induced arthritis by decreasing lipid peroxidation mediated oxidative stress by increasing the status of antioxidants in male Wistar rats
*BioAv↑, The encapsulation of thymol into methylcellulose microspheres by spray drying remarkably increases the bioavailability compared to free thymol
*Obesity↓, These findings indicate that Vitamin C can reduce obesity-associated cellular stress and thus provide a rationale for future investigations.
*ER Stress↓, Vitamin C prevented the increase in hypoxia (Fig. 1A–B), significantly reduced the induction of ER stress
*Inflam↓, nd ameliorated the increased expression of inflammatory genes
Hif1a↓, Vitamin C treatment for 24 and 48 h significantly reducing induction of HIF1α protein by 30–40% and VEGFA and GLUT1 mRNA by 40–80%
VEGF↓,
GLUT1↓,
GRP78/BiP↓, significantly reversing the effects of TNFα+PA pre-treatment only on GRP78 induction, by 30–40%
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*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, and neuroprotective mechanisms.
*Inflam↓,
*AntiCan↑,
*Bacteria↓,
*neuroP↑, cardiovascular protection, blood sugar regulation, anti-obesity, anticancer, antioxidant, anti-inflammatory, and neuroprotective properties.
*Obesity↓,
*cardioP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*ROS↓, Sprague-Dawley rat hearts, H9c2 cells 10 μM Reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential, and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria.
*MMP↑,
*ATP↑,
*MFN2↑,
*DRP1/DNM1L↓,
*FOXO3↑, Protect against DOX-induced acute cardiotoxicity Rats 30 mg/kg Vitexin induced elevated FOXO3a protein expression levels, by suppressing oxidative stress
*NRF2↑, vitexin activated nuclear factor-erythroid 2-related factor 2 (Nrf2) in HUVEC under high glucose.
*Ferroptosis↓, Diabetic nephropathy HK-2 cells/DN rat 0–40 μM Vitexin could alleviate diabetic nephropathy by attenuated ferroptosis via activating GPX4
*GPx4↑,
TumCP↓, Gastric cancer Nude mice/GC cells 2 mg/kg 10–160 μM Vitexin inhibited the malignant progression of GC in vitro and in vivo by suppressing HMGB1-mediated activation of PI3K/Akt/HIF-1α signaling pathway.
HMGB1↓,
PI3K↓,
Akt↓,
Hif1a↓,
CDK1↓, Colon cancer HCT-116 cells 1–300 μM Inhibit colon cancer HCT-116 cell proliferation by suppressing CDK1/cyclin B expression, leading to cell cycle arrest in the G2/M phase.
CycB/CCNB1↓,
TumCCA↑,
Apoptosis↑, Isovitexin Colon cancer Promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway.
P53↑,
NF-kB↓, Non-small cell lung cancer cells A549/ H1299 cells, nude mice 1–120 μM Suppressed NF-κB, AKT and ERK activation. [24] Vitexin A549 cells, nude mice 0–40 μM Reduced the levels of p-PI3K, p-Akt, and p-mTOR.
ERK↓,
p‑PI3K↓,
miR-34a↑, Isovitexin Hepatocarcinoma SK-Hep-1 cells Mediated miR-34a upregulation induces apoptosis and suppresses the stemness of SK-SC.
Apoptosis↑,
CSCs?,
*MAPK↓, Isovitexin Acute lung injury RAW 264.7 cells 0–50 μM Inhibiting MAPK and NF-κB and activating HO-1/Nrf2 pathways.
*HO-1↑,
*hepatoP↑, EAH mice 5 mg/kg Vitexin ameliorated hepatic injury in EAH mice through activation of the AMPK/AKT/GSK-3β pathway and upregulation of the Nrf2 gene.
*AMPK↑,
*Akt↑,
*GSK‐3β↑,
*chemoP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*Casp3↓,
*IRes↝, Vitexin and isovitexin flavonoids not only affected the absorption of peripheral glucose in insulin and non-insulin sensitive tissues but also showed the potential to restore insulin resistance in HepG2 cells by enhancing cellular uptake of glucose.
*GlucoseCon↑,
ChemoSen↑, When combined with doxorubicin (Dox), vitexin can reduce tumor growth and show synergistic effects in in vivo tests, increasing antitumor efficacy.
*GSH↑, Vitexin also increased Nrf2 expression and boosted GSH and antioxidant enzymes such as SOD, CAT, GPx, and GST.
*SOD↑,
*ATF2↑,
*GPx↑,
*GSTs↑,
*AntiAge↑, In Caenorhabditis elegans, studies have shown that vitexin and isovitexin, as putative SKN-1/Nrf2 activators, increase lifespan and support a healthy lifespan.
*Stroke↓, It has been demonstrated that vitexin protects against a cerebral ischemia/reperfusion (I/R)-induced increase in the permeability of brain endothelial cells
*AChE↓, vitexin treatment significantly inhibited acetylcholinesterase activity and markedly downregulated the expression of ace-1 and ace-2.
*ACE/ACE1↓,
*ACE2↓,
*GutMicro↑, Vitexin and isovitexin have also shown promising potential in modulating intestinal microbiota and in turn play a significant role in regulating various diseases such as overweight
*MPO↓, Vitexin can also resist Helicobacter pylori infection, which may be related to its anti-myeloperoxidase (MPO) enzyme activity and inhibition of H- and K-ATPase activity
*H+/K+-ATPase↓,
*AntiDiabetic↑, Antidiabetic Vitexin and Isovitexin Inhibits α-glucosidase/α-amylase, promotes GLUT4, modulates gut microbiota
*GLUT4↑,
*Obesity↓, Anti-obesity Vitexin Activates AMPKα, inhibits C/EBPα, FAS, activates Hedgehog signaling
*HH↓,
*RenoP↑, vitexin protects the kidneys and prevents the formation of kidney stones by inhibiting pyroptosis, apoptosis, epithelial–mesenchymal transition (EMT), and macrophage activation.
*BioAv↓, Vitexin and isovitexin have poor absorption in the gastrointestinal tract, with significant first-pass effects in the intestine (approximately 94%), stomach (30%), and liver (50%), resulting in a lower bioavailability (F) (approximately 5%).
*BioAv↝, The absorption and metabolism processes of vitexin and isovitexin in the human body are complex, and their bioavailability is influenced by multiple factors, including the action of the gut microbiota, interactions with dietary components, first-pass
*BioAv↑, The vitexin-loaded bilayer nanoparticles are designed by assembling soybean peptides and coating them with a goblet cell-targeting peptide. They significantly increase the bioaccessibility and bioavailability of vitexin
Showing Research Papers: 1 to 44 of 44
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 44
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CD47↓, 1, miR-124-3p↓, 1, PFS↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, CYP1A1↓, 1, GSH↑, 1, GSTs↑, 1, H2O2↑, 1, lipid-P↑, 1, NADH↓, 1, NRF2↓, 1, ROS↑, 7, i-ROS↑, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↑, 1, MMP↓, 5, MPT↑, 1, mtDam↑, 1, PGC-1α↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, SCD1↓, 1, SIRT1↓, 3,
Cell Death(tgid=5) ⓘ
Akt↓, 3, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↓, 1, Apoptosis↑, 9, BAX↑, 4, Bcl-2↓, 2, Bcl-2↑, 1, Casp↑, 1, Casp1↑, 1, Casp3↑, 5, Casp8↑, 1, Casp9↑, 3, Cyt‑c↑, 4, IAP2/BIRC3↓, 1, iNOS↓, 1, Mcl-1↓, 1, p38↑, 1, TRPV1↑, 2, TumCD↑, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
miR-25-5p↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
EZH2↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, GRP78/BiP↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 2, P53↓, 2, P53↑, 2, PARP↑, 2, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK4↓, 3, CycB/CCNB1↓, 2, cycD1/CCND1↓, 3, cycE/CCNE↓, 1, mitA↑, 1, P21↑, 2, TumCCA↑, 9,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs?, 1, EMT↓, 1, ERK↓, 4, GSK‐3β↓, 1, GSK‐3β↑, 1, miR-34a↑, 1, mTOR↓, 1, NOTCH↓, 1, PI3K↓, 4, p‑PI3K↓, 1, STAT3↓, 2, TOP1↓, 1, TOP2↓, 1, TumCG↓, 1,
Migration(tgid=13) ⓘ
BACH1↓, 1, Ca+2↑, 4, E-cadherin↓, 1, LAMs↓, 1, MALAT1↓, 1, MMP2↓, 3, MMP9↓, 3, MMPs↓, 1, PKCδ↓, 1, Smad1↓, 1, TGF-β↓, 1, TRIB3↑, 1, TumCI↓, 2, TumCMig↓, 6, TumCP↓, 6, TumMeta↓, 2, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, EGFR↓, 3, Hif1a↓, 5, VEGF↓, 4,
Barriers & Transport(tgid=15) ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 3, HMGB1↓, 1, IL6↓, 1, Imm↑, 2, Inflam↓, 1, NF-kB↓, 2, NK cell↑, 1, PD-1↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1, CDK6↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 4, ChemoSen↑, 7, Dose?, 1, Dose↝, 3, eff↑, 9, Half-Life↓, 1, Half-Life↑, 1, RadioS↑, 1, selectivity↑, 3,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, EGFR↓, 3, EZH2↓, 1, GutMicro↝, 1, IL6↓, 1, TRIB3↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, AntiTum↑, 3, cardioP↑, 1, chemoP↑, 4, chemoPv↑, 1, hepatoP↑, 1, NP/CIPN↓, 2, Obesity↓, 3, QoL↑, 1, radioP↑, 2, RenoP↑, 1, Risk↓, 1, toxicity↓, 1, TumVol↓, 2, Wound Healing↑, 1,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 1, CD8+↑, 2,
Total Targets: 140
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
ACE/ACE1↓, 1, ACE2↓, 1, AntiArt↑, 2, AntiBio↑, 3, compII↑, 1, diuretic↑, 1, H+/K+-ATPase↓, 1, IRes↓, 1, IRes↝, 1, PSEN1/PS1↓, 1, PSEN2/PS-2↓, 1, Stress↓, 1, Stroke↓, 5,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 3, antiOx↑, 19, Catalase↑, 8, Ferroptosis↓, 1, GPx↑, 11, GPx4↑, 1, GSH↑, 8, GSR↑, 2, GSTs↑, 2, H2O2↓, 1, HDL↑, 4, HDL∅, 1, HO-1↓, 1, HO-1↑, 4, Keap1↝, 1, lipid-P↓, 5, MDA↓, 8, MFN2↑, 1, MPO↓, 2, NADH↓, 1, NQO1↑, 2, NRF2↑, 10, RNS↓, 1, ROS?, 1, ROS↓, 21, mt-ROS?, 1, SOD↑, 12, mt-SOD↑, 1, TBARS↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↓, 1, ATP↑, 5, compIII↑, 1, DRP1/DNM1L↓, 1, Insulin↓, 1, Insulin↑, 1, Insulin↝, 1, MMP↑, 3, OCR↑, 1, PGC-1α↝, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
adiP↑, 1, ALAT↓, 4, AMPK↑, 2, glucose↓, 4, GlucoseCon↑, 1, HMG-CoA↓, 1, LDH↓, 1, LDL↓, 6, lipidLev↓, 1, PFK↓, 1, PPARγ↓, 1, PPARγ↑, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 2, ATF2↑, 1, Bcl-2↑, 1, Casp12↓, 1, Casp3↓, 2, Fas↓, 1, Ferroptosis↓, 1, GranB/GZMB↓, 1, iNOS↓, 2, p‑JNK↓, 1, MAPK↓, 3, MCT1↓, 1, necrosis↓, 1, p38↓, 1, p‑p38↓, 1, TRPV1↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↓, 2, other↑, 3, other↝, 3, PhotoS↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↓, 1, p‑eIF2α↓, 1, ER Stress↓, 2, GRP78/BiP↓, 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) ⓘ
DNAdam↓, 1, DNMT1↓, 1, PARP1↓, 1, γH2AX↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
FOXO3↑, 1, GSK‐3β↓, 3, GSK‐3β↑, 1, HH↓, 1, mTOR↓, 3, Nestin↑, 1, neuroG↑, 1, NOTCH1↑, 1, PI3K↓, 2, PI3K↑, 2, SOX2↑, 1, TRPM7↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, AntiAg↓, 1, AntiAg↑, 5, APP↓, 1, Ca+2↑, 1, Ki-67↑, 1, TGF-β↑, 1, TIMP1↓, 1, TumCP↓, 1, VCAM-1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, ATF4↓, 1, Hif1a↓, 1, NO↓, 3, VEGF↓, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↓, 2, BBB↑, 1, GastroP↑, 4, GLUT4↑, 1, IBI↑, 2, OCLN↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 1, COX1↓, 1, COX2/PTGS2↓, 5, COX2/PTGS2↑, 1, CRP↓, 1, ICAM-1↓, 1, IFN-γ↓, 1, IL10↓, 1, IL10↑, 1, IL12↓, 1, IL18↓, 1, IL1β↓, 5, IL4↓, 1, IL6↓, 7, IL8↓, 1, Imm↑, 10, Inflam↓, 27, LPS↓, 1, pol-M2 MC↑, 1, MCP1/CCL2↓, 1, MyD88↓, 1, NF-kB↓, 12, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 9, TNF-α↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, AChE↓, 7, BChE↓, 2, BDNF↑, 3, MAOA↓, 1, NGF↑, 2, tau↓, 2, p‑tau↓, 2, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 2, Aβ↓, 7, BACE/β-secretase↓, 4, MAOB↓, 1, NLRP3↓, 4, PP2A↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CYP19↓, 2, Leptin↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 10, BioAv↑, 21, BioAv⇅, 1, BioAv↝, 8, BioEnh↑, 2, Dose↝, 9, eff↑, 8, Half-Life↓, 1, Half-Life↑, 1, Half-Life↝, 2, P450↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 4, ALP↓, 1, AST↓, 6, BP↓, 4, creat↓, 1, CRP↓, 1, GutMicro↑, 18, IL6↓, 7, Ki-67↑, 1, LDH↓, 1, NOS2↓, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 9, AntiDiabetic↑, 19, antiPs↑, 2, AntiTum↑, 1, Appetite↓, 1, cardioP↑, 19, chemoP↑, 2, chemoPv↑, 1, cognitive↑, 7, hepatoP↑, 14, memory↑, 6, motorD↑, 1, neuroP↑, 23, Obesity↓, 42, OS↑, 1, Pain↓, 2, RenoP↑, 5, Risk↓, 1, toxicity↓, 12, toxicity↝, 2, Weight↓, 1, Wound Healing↑, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 2, Bacteria↓, 12, Sepsis↓, 2,
Total Targets: 223
Scientific Paper Hit Count for: Obesity, Obesity
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#:930 State#:% Dir#:1
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