TBARS Cancer Research Results

TBARS, Thiobarbituric Acid Reactive Substances: Click to Expand ⟱
Source:
Type: measure
TBARS (Thiobarbituric Acid Reactive Substances) is a measure of lipid peroxidation, which is the oxidative degradation of lipids. Lipid peroxidation is a process in which free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs), leading to cell damage.

Research has shown that TBARS levels are often elevated in cancer patients. This is because cancer cells have higher levels of reactive oxygen species (ROS) than normal cells, which can lead to increased lipid peroxidation.
Scientific Papers found: Click to Expand⟱
2657- AL,    Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases
- Review, CardioV, NA - Review, AD, NA
*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and γ-glutamyl cysteine synthetase (γ-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)

2660- AL,    Allicin: A review of its important pharmacological activities
- Review, AD, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2/PTGS2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2/KDR/Flk1↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,

7409- Amla,    Clinical evaluation of Emblica Officinalis Gatertn (Amla) in healthy human subjects: Health benefits and safety results from a randomized, double-blind, crossover placebo-controlled study
- Trial, Nor, NA
*HDL↑, a significant improvement in HDL-cholesterol and lowering the LDL-cholesterol levels.
*LDL↓,
*ROS↓, In conclusion, amla supplementation showed acceptable palatability, improved endothelial functions and reduced oxidative stress.
*AntiAg↑, Inhibition of platelet aggregation by oral supplementation of amla is attributable primarily to the abundance of low molecular weight (<1000 Da) hydrolysable ellagitannins
*TBARS↓, The oral administration of amla reduced TBARS levels in plasma, suggesting amla consumption could also ameliorate oxidative stress due to aging-related mitochondrion dysfunction.
*Dose↝, These results indicate the tolerance and safety of a daily 500 mg dose of amla in healthy humans

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↓,

2794- CHr,    An updated review on the versatile role of chrysin in neurological diseases: Chemistry, pharmacology, and drug delivery approaches
- Review, Park, NA - Review, Stroke, NA
*neuroP↑, chrysin has protective effects against neurological conditions by modulating oxidative stress, inflammation, and apoptosis in animal models.
*ROS↓,
*Inflam↓,
*Apoptosis↓,
*IL1β↓, attenuated IL-1β and TNF-α, COX-2, iNOS, and NF-kB expression, activated JNK
*TNF-α↓,
*COX2/PTGS2↓,
*iNOS↓,
*NF-kB↓,
*JNK↓,
*HDAC↓, alleviated histone deacetylase (HDCA) activity, GSK-3β levels, IFNγ, IL-17,
*GSK‐3β↓,
*IFN-γ↓,
*IL17↓,
*GSH↑, increased GSH levels
*NRF2↑, Park's: Increased Nrf2, modulated HO-1, SOD, CAT, decreased MDA, inhibited NF-κB and iNOS
*HO-1↑, upregulated expression of hallmark antioxidant enzymes, including HO-1, SOD, and CAT; and decreased levels of MDA
*SOD↑,
*MDA↓,
*NO↓, Attenuated NO, increased GPx
*GPx↑,
*TBARS↓, decreased levels of TBARS, AChE, restored activities of GR, GSH, SOD, CAT and Vitamin C
*AChE↓,
*GR↑,
*Catalase↑,
*VitC↑,
*memory↑, attenuated memory impairment
*lipid-P↓, attenuated lipid peroxidation
*ROS↓, attenuated ROS

7406- Chy,    Antiamnesic activity of an ayurvedic formulation chyawanprash in mice
- in-vivo, AD, NA
*Dose↝, beneficial effects of Chy (at the dose of 1 and 2% w/w of diet) administered daily for 15 successive days in mice with memory deficits.
*memory↑, The administration of Chy for 15 consecutive days significantly protected the animals from developing memory impairment.
*TBARS↓, there was a significant decrease in brain TBARS and increase in GSH levels after administration of Chy (2% w/w), thereby indicating decreased free radical generation and increased scavenging of free radical, respectively
*GSH↑,
*ROS↓,
*cognitive↑, Thus, Chy may prove to be a useful remedy for the management of Alzheimer's disease owing to its antioxidant effect, pro-cholinergic action and/or antiamnesic potential.
*AntiAge↑, Chy had been one of the most respected anti-ageing ayurvedic tonic, long before the clinical importance of vitamins, minerals and antioxidants was appreciated
*hepatoP↑, It is not only hepatoprotective but it also streamlines the metabolism of fats and proteins
*antiOx↑, It possesses promising antioxidant, cardiotonic, cholesterol lowering and anti-inflammatory properties
*LDL↓,
*Inflam↓,
*other↝, Chy is made in anwala base (Indian gooseberry, Emblica officinalis) [16], which is one of the richest sources of vitamin C (ascorbic acid)
*AChE∅, No statistically significant differences were observed in brain AChE activity of Chy-treated mice and control group mice.

6308- Cro,    Dietary Crocin is Protective in Pancreatic Cancer while Reducing Radiation-Induced Hepatic Oxidative Damage
- vitro+vivo, PC, Bxpc-3
Bcl-2↓, Crocin significantly reduced cell viability of BXPC3 and Capan-2 by triggering caspase signaling via the downregulation of Bcl-2.
Apoptosis↑, crocin treatment-induced apoptosis by inducing the release of cytochrome c from mitochondria to cytosol.
Cyt‑c↑,
TumCG↓, In mice bearing pancreatic tumors, crocin significantly reduced tumor burden without a change in body weight.
radioP↑, Additionally, it showed significant protection against radiation-induced hepatic oxidative damage, reduced the levels of hepatic toxicity and preserved liver morphology.
TumCCA↑, Various studies have shown that carotenoids of saffron extract, crocin and crocetin, arrest the cell cycle at S, G0/G1and G2/M stages [26,27,28,29,30,31,32,33,34], inhibiting mitosis, cell proliferation and triggering apoptosis.
TumCP↓,
DNAdam↑, crocin induces DNA fragmentation, apoptosis and cell cycle arrest at the G1 phase in Bx-PC-3 pancreatic cancer cells
TBARS↓, Crocin showed dose-dependent inhibition of TBARS
P53↑, Crocin upregulated P53, P38, cytochrome c, P21cip1 and P27kip1, whereas CDK2 and c-Myc were downregulated dose-dependently in BXPC3 and Capan-2 cells
p38↑,
CDK2↓,
cMyc↓,
*MDA↓, IR (4Gy) increased the MDA levels in mice and crocin treatment restores the MDA level
GSH↑, In this study, increased GSH level (Table 1) suggests that protection by the crocin mediated through the restoration of IR altered hepatic antioxidant status (Table 1 and Table 2).

6562- Ger,    Potential Effects of Geraniol on Cancer and Inflammation-Related Diseases: A Review of the Recent Research Findings
- Review, Var, NA - Review, AD, NA
*Inflam↓, wide spectrum of pharmacological activities including anti-inflammatory, anticancer, antimicrobial, antioxidant, and neuroprotective activities.
*AntiCan↑,
*AntiBio↑,
*antiOx↑,
*neuroP↑,
ROS↓, GNL scavenges free radicals and preserves the activity of antioxidant enzymes.
Apoptosis↑, GNL induces apoptosis and cell cycle arrest, modulates multiple molecular targets, including p53 and STAT3, activates caspases, and modulates inflammation via transcriptional regulation.
TumCCA↑,
P53↝,
STAT3↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
Casp↝,
*Catalase↑, This compound protects various antioxidant enzymes, such as catalase, glutathione-S-transferase, and glutathione peroxidase.
*GSTs↑,
*GPx↑,
*AChE↓, In addition, GNL suppressed acetylcholinesterase (AChE) activity and alleviated oxidative stress by boosting neuronal reduced glutathione (GSH), catalase (CAT), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities.
*GSH↑,
*SOD↑,
*TBARS↓, It lowered malondialdehyde concentration (TBARS), nitric oxide (NO), and xanthine oxidase (XO), and restored the structural damage to the brain tissue caused by HFD.
*NO↓,
*XO↓,
*memory↑, GNL boosted learning and memory function and ameliorated the inflammation status in the brain by lowering the protein levels of IL-1β, iNOS, NF-κBp65, and COX-2
*IL1β↓,
*iNOS↓,
*NF-kB↓,
*COX2/PTGS2↓,
*NRF2↑, GNL administration ameliorated renal function, alleviated histological changes, and enhanced Nrf-2/HO-1/NQO-1 with a subsequent intensification of antioxidant enzyme activities.
*HO-1↑,
*survivin↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
TumCP↓, They have shown that GNL treatment significantly suppressed oral squamous cell carcinoma (OSCC) cell proliferation and migration in vitro and tumor growth in vivo in a time- and dose-dependent manner.
TumCMig↓,
TumCG↑,
selectivity↑, GNL may be helpful in treating different types of malignancy, while having limited effects on normal cells.
TumMeta↓, GNL has been reported to inhibit cancer metastasis and angiogenesis.
angioG↓,
Hif1a↓, A549 lung cancer cells treated with GNL, downregulation of HIF-1alpha, a VEGF regulator, occurred
Beclin-1↓, GNL also decreases autophagy through downregulation of BNIP3 and beclin-1 expression, which increases apoptotic cell death through HIF-1α signaling.

7487- H2,    A comprehensive review of molecular hydrogen as a novel nutrition therapy in relieving oxidative stress and diseases: Mechanisms and perspectives
- Review, Nor, NA
*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↓,

7489- H2,    Molecular Hydrogen in the Treatment of Respiratory Diseases
- Review, Asthma, NA
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,

7879- isoO,    Isoorientin improves scopolamine-induced cognitive impairments by restoring the cholinergic system, antioxidant defense, and p-CREB/BDNF signaling in the hippocampus and frontal cortex
- in-vivo, AD, NA
*cognitive↑, ISO (5 and 10 mg/kg, p.o.) treatment significantly improved the cognitive impairments caused by scopolamine.
*AChE↓, ISO significantly decreased scopolamine-induced acetylcholinesterase and thiobarbituric acid reactive substance activities in both the hippocampus and frontal cortex of mice.
*TBARS↓,
*SOD↑, ISO significantly increased the levels of total superoxide dismutase induced by scopolamine in the hippocampus and frontal cortex.
*p‑CREB↑, ISO reversed the decreases in expression of phosphorylated cAMP response element binding (CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus and frontal cortex of scopolamine-treated mice.
*BDNF↑,
*memory↑, ISO ameliorates scopolamine-induced memory and cognitive impairments partly by restoring the cholinergic system, antioxidant defense, and p-CREB/BDNF signaling pathway, thereby exhibiting memory-enhancing activities.
*cognitive↑,


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   GSH↑, 1,   ROS↓, 1,   ROS↑, 2,   TBARS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 3,   Bak↓, 1,   BAX↑, 1,   Bcl-2↓, 3,   BID↑, 1,   Casp↝, 1,   Casp12↑, 1,   Casp3↑, 3,   Casp8↑, 2,   Casp9↑, 2,   Cyt‑c↑, 3,   Fas↑, 2,   p38↑, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

CHK1↓, 1,   DNAdam↑, 1,   P53↑, 3,   P53↝, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 4,  

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

FGF↓, 1,   STAT3↓, 2,   TumCG↓, 1,   TumCG↑, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

CEA↓, 1,   p‑FAK↓, 1,   TIMP2↑, 1,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↑, 1,   Hif1a↓, 2,   VEGF↓, 2,   VEGFR2/KDR/Flk1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL8↓, 1,   NF-kB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

CEA↓, 1,   EGFR↑, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   chemoP↑, 2,   QoL↑, 1,   radioP↑, 2,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 65

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 3,   SpO2↑, 1,   Stress↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 7,   Catalase↑, 5,   Fenton↓, 1,   GPx↑, 2,   GSH↑, 8,   GSTs↑, 2,   HDL↑, 2,   HO-1↑, 4,   Keap1↓, 1,   Keap1↑, 1,   lipid-P↓, 4,   MDA↓, 5,   MPO↓, 3,   NOX4↓, 1,   NRF2↑, 6,   RNS↓, 1,   ROS↓, 10,   SOD↑, 10,   TBARS↓, 10,   uricA↓, 1,   VitC↑, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   p‑CREB↑, 1,   H2S↑, 1,   LDH↓, 2,   LDL↓, 3,   NADPH↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 3,   BAX↓, 1,   Bcl-2↑, 2,   Bcl-xL↑, 1,   Casp3↓, 2,   Casp9↓, 1,   Cyt‑c↓, 1,   iNOS↓, 6,   JNK↓, 1,   p‑p38↓, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,   other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,   HSP70/HSPA5↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 2,   γH2AX↓, 1,  

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

GSK‐3β↓, 1,   HDAC↓, 1,   PI3K↓, 1,   PI3K↑, 1,   STAT3↑, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   MMP13↓, 1,   Treg lymp↝, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

p‑eNOS↑, 1,   NO↓, 3,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 3,   GastroP↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↑, 1,   CD4+↑, 2,   COX2/PTGS2↓, 5,   FOXP3↑, 1,   HMGB1↓, 1,   IFN-γ↓, 1,   IL10↑, 1,   IL17↓, 1,   IL1β↓, 4,   IL4↑, 1,   IL6↓, 3,   IL6↑, 1,   Imm↑, 1,   Inflam↓, 8,   JAK2↑, 1,   M2 MC↑, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 5,   PGE2↓, 2,   TNF-α↓, 6,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 4,   AChE∅, 1,   BChE↓, 1,   BDNF↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE/β-secretase↓, 1,   NLRP3↓, 1,   XO↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

GR↑, 1,   RAAS↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   Dose↓, 1,   Dose↑, 1,   Dose↝, 5,   eff↑, 4,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BP↓, 1,   creat↓, 2,   GutMicro↑, 2,   IL6↓, 3,   IL6↑, 1,   LDH↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   AntiTum↑, 1,   cardioP↑, 5,   cognitive↑, 5,   hepatoP↑, 3,   memory↑, 6,   motorD↑, 1,   neuroP↑, 7,   Obesity↓, 1,   OS↑, 1,   Pain↓, 1,   RenoP↑, 1,   toxicity↓, 2,   Weight↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   CD8+↑, 1,  
Total Targets: 132

Scientific Paper Hit Count for: TBARS, Thiobarbituric Acid Reactive Substances
2 Allicin (mainly Garlic)
2 Hydrogen Gas
1 Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry
1 α-Bisabolol / Chamomile oil
1 Chrysin
1 Chyawanprash
1 Crocetin
1 Geraniol
1 isoorientin
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#:862  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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