creat Cancer Research Results

creat, creatinine: Click to Expand ⟱
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Creatinine is fundamentally a metabolic waste product derived from creatine phosphate in muscle. Its blood levels are routinely used as a clinical biomarker to assess kidney function rather than a direct regulator of oncogenic processes.
Creatinine is a primary marker used to estimate the glomerular filtration rate (GFR).

-Elevated creatinine can be a sign of compromised kidney vascular function.
Scientific Papers found: Click to Expand⟱
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↓,

3456- ALA,    Renal-Protective Roles of Lipoic Acid in Kidney Disease
- Review, NA, NA
*RenoP↑, We focus on various animal models of kidney injury by which the underlying renoprotective mechanisms of ALA have been unraveled
*ROS↓, ALA’s renal protective actions that include decreasing oxidative damage, increasing antioxidant capacities, counteracting inflammation, mitigating renal fibrosis, and attenuating nephron cell death.
*antiOx↑,
*Inflam↓,
*Sepsis↓, figure 1
*IronCh↑, ALA can also chelate metals such as zinc, iron, and copper and regenerate endogenous antioxidants—such as glutathione—and exogenous vitamin antioxidants—such as vitamins C and E—with minimal side effects
*BUN↓, ALA can decrease acute kidney injury by lowering serum blood urea nitrogen, creatinine levels, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), thereby decreasing endothelin-1 vasoconstriction, neutrophil dif
*creat↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*MDA↓, pretreatment with ALA decreased MDA content and ameliorated renal oxidative stress
*NRF2↑, activate the Nrf2 signaling pathway, leading to upregulation of the second-phase cytoprotective proteins such as heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1)
*HO-1↑,
*NQO1↑,
*chemoP↑, ALA has also been shown to lower plasma creatinine levels and urine output, increase creatinine clearance and urine osmolality, and normalize sodium excretion in cisplatin kidney injury
*eff↑, ALA can also minimize renal toxicity induced by gold nanoparticles, which are often used as drug carriers
*NF-kB↓, Enhancing autophagy, inhibiting NF-KB, attenuating mitochondrial oxidative stress

3170- Ash,    Withaferin A protects against hyperuricemia induced kidney injury and its possible mechanisms
- in-vitro, Nor, NRK52E - in-vivo, NA, NA
*RenoP↑, WFA ameliorated renal damage, improved kidney function, and decreased levels of creatinine, BUN, UA, and XOD in PO-induced hyperuricemic mice.
*hepatoP↑,
*creat↓,
*BUN↓,
*uricA↓,
*Apoptosis↓, WFA markedly inhibited renal apoptosis, accompanied by changes of apoptosis-related proteins.
*α-SMA↓, Notably reduced α-SMA expression was observed after WFA administration, with WFA 10 mg/kg group presenting the most significant inhibitory effect.

3505- Bor,    Mineral requirements for mitochondrial function: A connection to redox balance and cellular differentiation
- Review, NA, NA
*glucose↓, Boron supplementation in human subjects decreased serum glucose, creatinine, and calcitonin,
*creat↓,
*SOD↑, while it increased serum triglycerides, ceruloplasmin, and erythrocyte superoxide dismutase
*MMP↑, Boron administration had positive effects on mitochondrial membrane potential and function in multiple species, but entry into mitochondria was not confirmed
*ROS↓, The available evidence suggest that mitochondria may benefit from the availability of boron, which may promote metabolism and reduce redox stress.

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↓,

5898- CAR,    Carvacrol-induced apoptosis via tumor suppressor gene activation and oxidative stress modulation in a rat model of breast cancer
- in-vivo, BC, NA
*lipid-P↓, Carvacrol also attenuated lipid peroxidation by reducing malondialdehyde (MDA) levels, while boosting total antioxidant capacity and improving inflammatory status.
*MDA↓,
*antiOx↑,
*Inflam↑,
RenoP↑, Moreover, restoration of liver and kidney function was observed through normalization of serum ALT, AST, urea, and creatinine levels
hepatoP↑,
*ALAT↓,
AST↓,
creat↓,
chemoPv↑, Preclinical studies have demonstrated the chemopreventive and therapeutic potential of Carvacrol in several malignancies, including breast cancer, melanoma, hepatocellular carcinoma, cervical cancer, and non-small cell lung cancer
Cyt‑c↑, markedly enhanced cytochrome c expression
FADD↑, . Carvacrol-injected therapy markedly elevated FADD expression
P53↑, Carvacrol receiving rat’s up-regulated P53 concentrations markedly that reached their peak in the injected (## P ≤ 0.01 vs. tumor and **P ≤ 0.01 vs. normal) as well as oral and mixed groups

6282- DL,    Limonene Exerts Anti-Inflammatory Effect on LPS-Induced Jejunal Injury in Mice by Inhibiting NF-κB/AP-1 Pathway
- in-vivo, IBD, NA
*RenoP↑, pretreatment with limonene at doses of 100 and 200 mg/kg mitigated this decline in renal function, evidenced from the reduced levels of serum urea and creatinine.
*creat↓,
*Inflam↓, Limonene demonstrated anti-inflammatory effects by reducing pro-inflammatory cytokines (TNF-α, IL-1β, COX-2), suppressing the TLR4/NF-κB/AP-1
*TNF-α↓,
*IL1β↓,
*COX2/PTGS2↓,
*ROS↓, modulating oxidative stress through Nrf2 activation.
*NRF2↑,
*GastroP↑, mitigating intestinal inflammation and preserving gastrointestinal health.
*TLR4↓, suppressing the TLR4/NF-κB/AP-1
*NF-kB↓,
*AP-1↓,
*Sepsis↓, limonene has the potential to mitigate the severity of sepsis in mice.

6347- DRE,    Protective Effects of Taraxacum officinale L. (Dandelion) Root Extract in Experimental Acute on Chronic Liver Failure
*hepatoP↑, reduced serum liver injury markers (AST, ALT, ALP, GGT, total bilirubin), renal tests (creatinine, urea), and oxidative stress tests (TOS, OSI, MDA, NO, 3NT).
*AST↓,
*ALAT↓,
*ALP↓,
*Bil↓,
*creat↓,
*TOS↑,

6353- DRE,  Cisplatin,    Insights Into Protective Mechanisms of Dandelion Leaf Extract Against Cisplatin-Induced Nephrotoxicity in Rats: Role of Inhibitory Effect on Inflammatory and Apoptotic Pathways
- in-vivo, Nor, NA
*antiOx↑, Several studies demonstrated the antioxidant, anti-inflammatory, and antiapoptotic effects of dandelion leaf extract (DLE);
*Inflam↓,
*Apoptosis↓,
*NF-kB↓, DLE reduced nuclear factor-κB and cytochrome c expression, and DNA fragmentation
*Cyt‑c↓,
*DNAdam↓,
*GSH↑, also maintained levels of reduced glutathione, superoxide dismutase, and serum albumin.
*SOD↑,
*Albumin↝,
*creat↓, Treatment with DLE + CP maintained the levels of creatinine at all different DLE doses.
*BUN↓, Treatment with DLE + CP significantly ameliorated the elevated levels of creatinine and BUN.
*RenoP↑, These results demonstrate that DLE administration protected the kidney from renal injury that could occur by CP injection.
*lipid-P↓, The DLE pretreated rats showed a significant decline in LPO levels compared to that observed with CP treatment alone
*TNF-α↓, DLE alone decreased the levels of TNF-α by 15% of control levels. Rats treated with DLE prior to CP exhibited a significant (P < .001) suppression in the levels of TNF-α compared to CP-treated rats.
*Casp3↓, animals treated with DLE prior to CP administration showed significant decrease in caspase-9 and caspase-3 to levels comparable to the control and compared to rats treated with CP alone
*Casp9↓,
*chemoP↑, nephroprotective activity of DLE against CP-induced nephrotoxicity.

4022- FulvicA,  Chemo,    Shilajit potentiates the effect of chemotherapeutic drugs and mitigates metastasis induced liver and kidney damages in osteosarcoma rats
- in-vivo, OS, NA
AST↓, Co-treatment of shilajit and drug cocktails also markedly alleviated histopathological changes in liver and kidney tissues.
ALAT↓, (AST)* and alanine aminotransferase (ALT), alkaline phosphatase (ALP), total proteins, albumin, bilirubin, creatinine, urea, and uric acid.
ALP↓,
Bil↝,
creat↓,
uricA↓,
ChemoSen↑, shilajit may potentiate the effects of chemotherapy drugs and mitigate the metastasis-induced liver and kidney damage in osteosarcoma.
chemoP↑,

7049- GA,    Pharmacological effects of gallic acid in health and diseases: A mechanistic review
- Review, Var, NA
*antiOx↑, Several beneficial effects are reported for gallic acid, including antioxidant, anti-inflammatory, and antineoplastic properties.
*Inflam↓,
*antiNeop↑,
*cardioP↑, reported to have therapeutic activities in gastrointestinal, neuropsychological, metabolic, and cardiovascular disorders
*Bacteria↓, Antimicrobial activity
*AST↓, Beryllium-induced hepatorenal toxicity ↓AST, ALT, ALP, LPO, AMND, ↑GSH, CAT, SOD, GPx & GST, ↓Cr & urea
*ALAT↓,
*ALP↓,
*lipid-P↓,
*GSH↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
*Urea↓,
*creat↓,
tumCV↓, human NCSLC NCI-H460 cells In vivo: mouse NCI-H460 xenograft model In vitro: ↓viability, induction of G2/M phase cell cycle arrest, ↑intracellular Ca2+, CDK1 activity, caspase-3, caspase-8 & caspase-9 activation, ↓ΔΨ
TumCCA↑,
i-Ca+2↑,
CDK1↑,
Casp3↑,
Casp8↑,
Casp9↑,
MMP↓,
ROS↑, In vitro: induction of S phase cell cycle arrest ↑ROS
MMPs↓, it can inhibit the invasion and metastasis by decreasing the matrix metalloproteinase expression and activity
*GastroP↑, Beside the gastroprotective activity, gallic acid ameliorates the hepatotoxic effects of xenobiotic agents by acting as an antioxidant compound that scavenges free radicals, such as ROS
*hepatoP↑,
*ROS↓,
*AChE↑, Gallic acid is also able to reverse the scopolamine-induced amnesia in mice, probably through inhibiting oxidative stress and decreasing acetylcholinesterase (AChE) enzyme activity in the brain

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

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

7492- H2,  Chemo,    Molecular Hydrogen Protects against Various Tissue Injuries from Side Effects of Anticancer Drugs by Reducing Oxidative Stress and Inflammation
- Review, Var, NA
*ROS↓, reduces reactive oxygen species, which have very strong oxidative capacity, and indirectly exerts antioxidant, anti-inflammatory
*antiOx↑,
*Inflam↓,
*chemoP↑, Our comprehensive literature review revealed that H2 protects against tissue injuries induced by cisplatin, oxaliplatin, doxorubicin, bleomycin, and gefitinib.
AntiCan↑, Animal and clinical studies showed that H2 itself exhibits anticancer activity, and its combination with anticancer drugs achieved excellent anticancer activity
ChemoSen↑,
chemoP↑, Our literature review revealed that H2 reduced the side effects of CIS-induced nephrotoxicity, ototoxicity, and ovarian injury, CIS- or OXA-induced peripheral neuropathy, DXR-induced cardiotoxicity and hepatotoxicity, and BLM- or GEF-induced lung inj
*BUN↓, CIS Nephrotoxicity BUN ↓, Creatinine ↓, TUNEL ↓
*creat↓,
*TUNEL↓,
*MDA↓, CIS Ototoxicity MDA ↓, 8-iso-PGF2α ↓
*SOD↑, CIS Ovarian injury SOD ↑, CAT ↑, MDA ↓, Nrf2 ↑
*Catalase↑,
*NRF2↑,
*BNP↓, DXR Cardiotoxicity and hepatotoxicity BNP ↓, AST ↓, ALT ↓, ROS ↓, MDA ↓, TNF-α ↓, IL-1β ↓, IL-6 ↓, TUNEL ↓, Bax/Bcl-2 ↓, Caspase-3 ↓, Caspase-8 ↓
*AST↓,
*ALAT↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*Casp3↓,
*Casp9↓,
*GPx↑, BLM Lung injury ROS ↓, MDA ↓ TGF-β1 ↓,TNF-α ↓, GSH-PX ↑, E-cadherin ↑, Vimentin ↓, α-SMA ↓, Collagen I ↓
*E-cadherin↑,
*Vim↓,
*α-SMA↓,
*COL1↓,
*cardioP↑, H2 ameliorated DXR-induced cardiotoxicity and hepatotoxicity by attenuating inflammation and apoptosis.
*hepatoP↑,
*p‑mTOR↓, decreased the phosphorylated mammalian target of rapamycin (p-mTOR) to mTOR
*EMT↓, H2 gas also inhibited BLM-mediated epithelial-to-mesenchymal transition by increasing the expression level of the epithelial cell marker E-cadherin and decreasing that of the mesenchymal cell marker vimentin [
eff∅, On the other hand, H2 did not impair the anticancer effects of GEF in in vitro experiments on lung cancer cell lines or in in vivo experiments on carcinoma-bearing mice
*LPS↓, figure 2
*TLR4↓,
radioP↑, radioprotective effects of H2 have also been reported in many in vitro and in vivo studies, and clinical trials recently showed that the inhalation of H2 gas mitigated decreases in quality of life and bone marrow damage associated with radiation [

7366- HibSad,    Does consumption of an aqueous extract of Hibscus sabdariffa affect renal function in subjects with mild to moderate hypertension?
- Human, Nor, NA
*creat↓, HS significantly increased (P < 0.001) creatinine clearance compared to placebo whereas lisinopril did not.
*RenoP↑, HS consumption improved indices of renal function in our study population of Nigerians with mild to moderate hypertension.

7890- IVT,    Isovitexin protects against cisplatin-induced kidney injury in mice through inhibiting inflammatory and oxidative responses
- in-vivo, Nor, NA
RenoP↑, renoprotective effects and mechanism of isovitexin, a glycosylflavonoid isolated from rice hulls of Oryza sativa, against cisplatin-induced kidney injury in mice.
*BUN↓, isovitexin inhibited CP-induced increases in serum BUN and creatinine.
*creat↓,
*TNF-α↓, Isovitexin inhibited CP-induced inflammation by inhibiting TNF-α, IL-1ß and IL-6 production in kidney tissues.
*IL1β↓,
*IL6↓,
*MDA↓, isovitexin inhibited CP-induced oxidative stress by inhibiting MDA and ROS production.
*ROS↓,
*NF-kB↓, isovitexin was found to inhibit CP-induced NF-κB activation and increase Nrf2 and HO-1 expression.
*NRF2↑,
*HO-1↑,

3264- Lyco,    Pharmacological potentials of lycopene against aging and aging‐related disorders: A review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
*antiOx↑, Anti‐oxidative mechanism of lycopene
*ROS↓, Lycopene inhibits ROS generation and subsequent oxidative stress by inducing antioxidant enzymes (SOD, CAT, GSH, GSH‐Px, and GST) and limiting MDA level and lipid peroxidation (LPO).
*SOD↑,
*Catalase↑,
*GSH↑,
*GSTs↑,
*MDA↓,
*lipid-P↓,
*NRF2↑, Lycopene also prevents ROS release by upregulating Nrf2‐mediated HO‐1 levels and inhibiting iNOS‐activated NO generation
*HO-1↑,
*iNOS↓,
*NO↓,
*TAC↑, upregulating total antioxidant capacity (TAC) and direct inhibition of 8‐OHdG, NOX4.
*NOX4↓,
*Inflam↓, Anti‐inflammatory mechanism of lycopene.
*IL1↓, IL‐1, IL‐6, IL‐8, IL‐1β, and TNF‐α release.
*IL6↓,
*IL8↓,
*IL1β↓,
*TNF-α↓,
*TLR2↓, prevents inflammation by inhibiting toll‐like receptors TLR2 and TLR4 and endothelial adhesion molecules VCAM1 and ICAM‐1.
*TLR4↓,
*VCAM-1↓,
*ICAM-1↓,
*STAT3↓, inhibiting STAT3, NF‐κB, ERK pathway, and IL‐6 and TNF‐α release.
*NF-kB↓,
*ERK↓,
*BP↓, Another clinical study demonstrated that consumption of raw tomato (200 g/day) could prevent type 2 diabetes‐associated cardiovascular diseases by lowering systolic and diastolic blood pressure, upregulating ApoA1, and downregulating ApoB levels
ROS↓, lycopene suppresses the metastasis of the SK‐HEP‐1 cell line by NOX‐4 mRNA expression inhibition and the reactive ROS intracellular activity inhibition
PGE2↓, Lycopene is also used to treat colorectal cancer cells in humans, and the introduction of lycopene decreases the prostaglandin E2 and nitric oxide levels
cardioP↑, Lycopene‐rich foods can be highly beneficial in preventing cardiovascular diseases as lycopene is a potential source of antioxidants
*neuroP↑, beneficial role of lycopene on aging‐related neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, has been confirmed in both experimental and clinical trials
*creat↓, Several pre‐clinical studies reported that lycopene treatment significantly reduced serum urea and serum creatinine, as well as reversed various toxic chemical‐induced nephrotoxicity and oxidative damage by exhibiting excellent antioxidative properti
*RenoP↑,
*CRM↑, its potency in treating aging disorders and its role as a mimic of caloric restriction.

3842- Moringa,    Bioactive Components in Moringa Oleifera Leaves Protect against Chronic Disease
- Review, Var, NA - Review, AD, NA
*antiOx↑, rich in antioxidants
*ROS↓, MO leaves also protect against oxidative stress [14], inflammation [15], hepatic fibrosis [16], liver damage [17], hypercholesterolemia [18,19], bacterial activity [20], cancer [14] and liver injury [21].
*hepatoP↑, methanol extract of MO leaves has a hepatoprotective effect, which might be due to the presence of quercetin
*lipid-P↓, reductions in lipids and lipid peroxidation levels in the liver of rats
*ALAT↓, MO leaves have been shown to reduce plasma ALT, AST, ALP and creatinine [82,83] and to ameliorate hepatic and kidney damage induced by drugs.
*AST↓,
*ALP↓,
*creat↓,
*RenoP↑,
NF-kB↓, MO was shown to contain the growth of pancreatic cancer cells, by inhibiting NF-ĸB signaling as well as increasing the efficacy of chemotherapy, by enhancing the effect of the drug in these cells
ChemoSen↑,
*memory?, MO, have been demonstrated to enhance memory by nootropics activity and protect against the oxidative stress present in AD

2933- NAD,    Nicotinamide mononucleotide (NMN) as an anti-aging health product – Promises and safety concerns
- Review, Nor, NA - NA, AD, NA - NA, Diabetic, NA - NA, Stroke, NA - NA, LiverDam, NA - NA, Park, NA
*mtDam↓, The mitochondrial decay, which is responsible for aging, can be reversed by the increased levels of nicotinamide adenine dinucleotide (NAD+) in the body.
*BioAv↝, NMN is a precursor of NAD+ that acts as an intermediate in NAD+ biosynthesis, while dietary supplements of NMN are found to increase the NAD+ levels in the body
*BioAv↑, molecular weight is 334.22 g/mol. It is fairly acidic and water-soluble compound. The solubility has been reported to be 1.8 mg/mL
*OS↑, plays a vital role in a variety of biological processes of the body including cell death, aging, gene expression, neuroinflammation and DNA repair, which indicating a significance role of NAD+ in longevity and health of human life
*eff↑, NMN has therapeutic effects towards a range of diseases, including age-induced type 2 diabetes, obesity, cerebral and cardiac ischemia, heart failure and cardiomyopathies
*eff↑, Alzheimer’s disease and other neurodegenerative disorders, corneal injury, macular degeneration and retinal degeneration, acute kidney injury and alcoholic liver disease
*cognitive↑, cognitive impairments, DNA damage and sirtulin gene inactivation, are brought about by aging which can be evaded by enhancing NAD+ count in the body
*DNAdam↓,
*SIRT1↑, NMN, the NAMPT reaction product, is able to be utilised to trigger the SIRT1 activity
*cardioP↑, NMN also can restore gene expression linked to circadian rhythm, inflammatory response and oxidative stress, and improve hepatic insulin sensitivity, partially by SIRT1 activation.
*ROS↓, NMN has been proven to reduce DNA damage and accumulation of ROS
*Dose↝, NMN in available commercial products vary from 50 to 150 mg/capsule, whereas some consumers take two 150 mg capsules per day
*BioAv↑, NMN was speedily absorbed in the small intestine by a specific transporter, which was encoded by the Slc12a8 gene as demonstrated in in vitro and in vivo studies
*hepatoP↑, NMN supplementation has been found to have significant recovering effects on hepatocyte functions and liver pathologies in early-stage of ethanol toxicity, instead of causing adverse effects to the liver
*eff↑, supplementation of NMN has been found to be a promising therapeutic remedy for PD
*BG↓, Oral administration of NMN increased serum bilirubin contents and decreased blood glucose, chloride and serum creatinine levels, but within the normal range.
*creat↓,

3014- RosA,    Rosmarinic Acid Supplementation Acts as an Effective Antioxidant for Restoring the Antioxidation/Oxidation Balance in Wistar Rats with Cadmium-Induced Toxicity
- in-vivo, Nor, NA
*antiOx↑, Rats in Group 4 (cadmium-exposed and Rosmarinic acid-accessed) exhibited increased levels of total proteins, a significant increase in the levels of antioxidant markers including total thiols, glutathione, total antioxidant capacity (TAC),
*Thiols↑,
*GSH↑,
*TAC↑, decreased levels of total thiols, GSH, catalase, and TAC
*SOD↑, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase, and a significant decrease in the levels of blood cadmium, ALP, ALT, AST, creatinine, blood urea nitrogen (BUN), urea, bilirubin, and oxidation markers (H2O2, and MDA
*GPx↑,
*Catalase↑,
*ALP↓,
*ALAT↓,
*AST↓,
*creat↓,
*BUN↓,
*H2O2↓,
*MDA↓,
*ROS↓, significantly help attenuate the oxidative stress induced by cadmium
cardioP↑, benefits of RA are attributed to its anti-cancer, anti-depressive, antiallergic, anti-inflammatory, anti-angiogenic, cardioprotective, hepatoprotective, nephroprotective, neuroprotective, antimicrobial, hypoglycemic, and hypolipidemic bioactivities
hepatoP↑,
neuroP↑,

4755- Se,  Chemo,    Selenium Prevention of Alopecia, Bladder and Kidney Toxicity Induced by Chemotherapeutic Agents
- in-vitro, Var, NA
chemoP↑, Researchers at Roswell Park Comprehensive Cancer Center have demonstrated that selenium containing compounds are highly effective in preventing alopecia and severe bladder toxicity associated with cyclophosphamide as well as in preventing kidney toxi
creat↓, significant increase in creatinine and blood urea nitrogen (BUN) following treatment with cisplatin were restored to normal values in animals that were treated.
BUN↓,

4453- SeNPs,    Selenium Nanoparticles: Green Synthesis and Biomedical Application
- Review, NA, NA
*toxicity↓, “Green” synthesis has special advantages due to the growing necessity for environmentally friendly, non-toxic, and low-cost methods.
*Bacteria↓, SeNPs are active against both Gram-positive and Gram-negative microorganisms
ROS↑, The cancer cells exhibit an acidic pH and an imbalanced redox state. These conditions in cancer cells initiate the pro-oxidant conversion of SeNPs and trigger the development of free radicals in malignant cells
MMP↓, mitochondrial membrane destruction
ER Stress↑, on the other hand, to stress in the endoplasmic reticulum (ER)
P53↑, Selenium nanoparticles can stimulate p53 expression in cancer cells, leading to caspase-9 activation, mitochondrial membrane potential depletion, and the induction of apoptosis.
Apoptosis↑,
Casp9↑,
DNAdam↑, In addition, in cellular processes, DNA structure is damaged, causing the cell cycle to stop and, ultimately, cell death.
TumCCA↑,
eff↑, positively charged SeNPs may have a strong affinity for breast cancer cells, causing the enhanced anticancer efficacy of SeNPs
Catalase↓, was accompanied by a decrease in antioxidant marker levels (CAT, SOD, GPx activity and GSH levels) in MCF-7 cells exposed to green SeNPs
SOD↓,
GSH↓,
selectivity↓, in contrast to control cells
selectivity↑, SeNPs selectively affect LDH leakage and membrane disruption in cancer cells because the SeNP concentration required to influence LDH leakage in normal cells is much higher compared to that in cancer cells
PCNA↓, SeNPs reduced the PCNA expression level in MCF-7 cells, showing their role in suppressing oncogenesis and proliferation in breast cancer by inhibiting PCNA gene expression
eff↑, Nanoparticle capping can enhance their absorption via accumulation by endocytosis in cancer cells, which can therefore lead to ROS generation induction
*ALAT↓, SeNPs could significantly decrease hepatic (serum ALT, AST, and ALP) and renal (serum uric acid, urea, and creatinine) function markers, total lipid, total cholesterol, triglyceride and low-density lipoprotein cholesterol levels, and glucose-6-phosph
*AST↓,
*ALP↓,
*creat↓,
*Inflam↓, selenium nanoparticles appear to be a possible anti-inflammatory agent.
*toxicity↓, Most studies confirm that SeNPs are less toxic than sodium selenite
selectivity↑, despite affecting cancer cells and causing their death, SeNPs do not harm normal cells,

3313- SIL,    Silymarin attenuates post-weaning bisphenol A-induced renal injury by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 signaling modulation in male Wistar rats
- in-vivo, NA, NA
*NRF2↑, silymarin activates the Nrf2/HO-1 pathway, thus providing cellular defense
*HO-1↑,
*creat↓, Silymarin diminished BPA-induced rise in serum urea, creatinine, BUN, and plasma kim-1 levels.
*BUN↓,
*RenoP↑, improved renal histoarchitecture in BPA-exposed rats.
*MDA↓, suppression of BPA-induced rise in renal iron, MDA, TNF-α, IL-1β, and cytochrome c levels, and myeloperoxidase and caspase 3 activities by silymarin therapy.
*TNF-α↓,
*IL1β↓,
*Cyt‑c↓,
*Casp3↓,
*GSTs↓, silymarin attenuated BPA-induced downregulation of Nrf2 and GSH levels, and HO-1, GPX4, SOD, catalase, GST, and GR activities.
*GSH↑,
*GPx4↑,
*SOD↑,
*GSR↓,
*Ferroptosis↓, silymarin mitigated post-weaning BPA-induced renal toxicity by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 modulation.

4126- Silicon,  H2,    Oral Administration of Si-Based Agent Attenuates Oxidative Stress and Ischemia-Reperfusion Injury in a Rat Model: A Novel Hydrogen Administration Method
- in-vivo, NA, NA
*creat↓, serum creatinine and urine protein were significantly decreased 72 h following IRI in rats that were administered nano-Si.
*ROS↓, oral nano-Si intake downregulated the biological processes related to oxidative stress, such as immune response, cytokine production, and extrinsic apoptotic signaling pathway.
*other↑, oral administration of nano-Si, which should be considered as a novel H2 administration method.
*MDA↓, Additionally, the serum malondialdehyde levels were significantly decreased in the IRI + nano-Si group compared
*other↑, new strategy to successfully generate large amounts of H2 molecules by crushing Si to nano-sized particles and allowing these nanoparticles to react with alkaline water.
*Inflam↓, H2 has been shown to exert anti-inflammatory and anti-apoptotic effects by suppressing oxidative stress

2113- TQ,    Potential role of Nigella sativa (NS) in abating oxidative stress-induced toxicity in rats: a possible protection mechanism
- in-vivo, Nor, NA
*antiOx↑, NS exhibited an anti-oxidative stress effect in the liver and kidneys as indicated by the low levels of ALT and creatinine.
*RenoP↑,
*hepatoP↑, studies have suggested a hepatoprotective effect of NS
*SOD↑, increase in SOD and GSH-Px indirectly caused an alleviation of oxidative stress, leading to a much lower level of MDA.
*GSH↑, decrease in SOD and G-Px levels were observed in a very short duration (peaked at the 3rd day of administration) and decreased to normal levels immediately after this period
*ROS↓, NS at 100 mg/kg b.w/per day for three consecutive days, demonstrated the highest efficacy in abating oxidative stress in rats.
*lipid-P↓, abating oxidative stress and lipid peroxidation in NS-treated group
ALAT↓,
creat↓,

2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, BUN, creatinine, CK and pro-inflammatory cytokines like TNF-α, IL-6 and MRP-1 to be elevated in the cisplatin-treated group while reducing glomerular filtration rate. Tq + Cur treatment significantly improved these conditions.
*TNF-α↓,
*IL6↓,
*MRP↓,
*GFR↑,
*mt-ATPase↑, antioxidant enzyme levels and mitochondrial ATPases were restored upon treatment,
*p‑Akt↑, Tq + Cur treatment increased the expressions of phosphorylated Akt, Nrf2 and HO-1 proteins while decreasing the levels of cleaved caspase 3 and NFκB in kidney homogenates.
*NRF2↑,
*HO-1↑,
*Casp3↓,
*NF-kB↓,
*RenoP↑, In summary, Tq + Cur had protective effects on cisplatin-induced nephrotoxicity and renal injury


Showing Research Papers: 1 to 26 of 26

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 26

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

BHB↑, 1,   CD47↓, 1,   HMGCS2↑, 1,   miR-124-3p↓, 1,   PFS↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Bil↝, 1,   Catalase↓, 1,   GSH↓, 2,   ROS↓, 1,   ROS↑, 3,   SOD↓, 1,   uricA↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 2,   PGC-1α↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   BUN↓, 1,   SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 3,   Bak↓, 1,   BAX↑, 1,   Bcl-2↓, 2,   BID↑, 1,   Casp12↑, 1,   Casp3↑, 3,   Casp8↑, 3,   Casp9↑, 4,   Cyt‑c↑, 3,   FADD↑, 1,   Fas↑, 2,   IAP2/BIRC3↓, 1,   p38↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

CHK1↓, 1,   DNAdam↑, 1,   P53↑, 4,   PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↑, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 4,  

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

FGF↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

i-Ca+2↑, 1,   CEA↓, 1,   p‑FAK↓, 1,   MALAT1↓, 1,   MMPs↓, 1,   TIMP2↑, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

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

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL8↓, 1,   NF-kB↓, 1,   NF-kB↑, 1,   NK cell↑, 1,   PGE2↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   ALP↓, 1,   AST↓, 2,   Bil↝, 1,   CEA↓, 1,   creat↓, 4,   EGFR↑, 1,   EZH2↓, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   cardioP↑, 2,   chemoP↑, 6,   chemoPv↑, 1,   hepatoP↑, 2,   neuroP↑, 1,   NP/CIPN↓, 1,   QoL↑, 1,   radioP↑, 2,   RenoP↑, 3,   TumVol↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 2,  
Total Targets: 98

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 2,   compII↑, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 13,   Bil↓, 1,   Catalase↑, 7,   Ferroptosis↓, 1,   GPx↑, 4,   GPx4↑, 1,   GSH↑, 9,   GSR↓, 1,   GSTs↓, 1,   GSTs↑, 3,   H2O2↓, 1,   HO-1↑, 6,   Keap1↓, 1,   Keap1↑, 1,   lipid-P↓, 8,   MDA↓, 11,   MFN2↑, 1,   MPO↓, 2,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 9,   ROS↓, 17,   SOD↑, 11,   TAC↑, 2,   TBARS↓, 2,   Thiols↑, 1,   TOS↑, 1,   uricA↓, 2,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 3,   compIII↑, 1,   MMP↑, 4,   mtDam↓, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 9,   BUN↓, 8,   CRM↑, 1,   glucose↓, 1,   H2S↑, 1,   KeyT↝, 1,   LDH↓, 2,   LDL↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↑, 1,   Apoptosis↓, 3,   BAX↓, 1,   Bcl-2↑, 1,   Casp12↓, 1,   Casp3↓, 5,   Casp9↓, 2,   Cyt‑c↓, 3,   Ferroptosis↓, 1,   GranB/GZMB↓, 1,   iNOS↓, 4,   p‑JNK↓, 1,   p38↓, 1,   TUNEL↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 4,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 2,  

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

EMT↓, 1,   ERK↓, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   PI3K↓, 1,   PI3K↑, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   APP↓, 1,   mt-ATPase↑, 1,   COL1↓, 1,   E-cadherin↑, 1,   MMP13↓, 1,   TGF-β↑, 1,   VCAM-1↓, 1,   Vim↓, 1,   α-SMA↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1,   NO↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   GastroP↑, 3,   IBI↑, 1,   MRP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 2,   COX2/PTGS2↓, 4,   ICAM-1↓, 1,   IFN-γ↓, 1,   IL1↓, 1,   IL10↑, 1,   IL1β↓, 8,   IL2↓, 1,   IL4↓, 1,   IL6↓, 9,   IL6↑, 1,   IL8↓, 1,   Imm↑, 2,   Inflam↓, 12,   Inflam↑, 1,   LPS↓, 2,   MCP1/CCL2↓, 1,   NF-kB↓, 7,   PGE2↓, 1,   TLR2↓, 1,   TLR4↓, 3,   TNF-α↓, 13,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   AChE↑, 1,   BChE↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,   BACE/β-secretase↓, 2,   NLRP3↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

BNP↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 4,   BioAv↝, 2,   Dose↝, 3,   eff↑, 7,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 9,   Albumin↝, 1,   ALP↓, 5,   AST↓, 8,   BG↓, 1,   Bil↓, 1,   BP↓, 2,   creat↓, 22,   GutMicro↑, 2,   IL6↓, 9,   IL6↑, 1,   LDH↓, 2,   Urea↓, 2,  

Functional Outcomes(tgid=23) ⓘ

antiNeop↑, 1,   antiPs↑, 1,   cardioP↑, 7,   chemoP↑, 3,   cognitive↑, 3,   GFR↑, 1,   hepatoP↑, 10,   memory?, 1,   memory↑, 1,   motorD↑, 1,   neuroP↑, 6,   Obesity↓, 1,   OS↑, 1,   Pain↓, 1,   RenoP↑, 12,   toxicity↓, 3,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   Bacteria↓, 2,   CD8+↑, 1,   Sepsis↓, 3,  
Total Targets: 160

Scientific Paper Hit Count for: creat, creatinine
4 Hydrogen Gas
3 Cisplatin
3 Chemotherapy
2 Dandelion Root
2 Thymoquinone
1 Allicin (mainly Garlic)
1 Alpha-Lipoic-Acid
1 Ashwagandha(Withaferin A)
1 Boron
1 α-Bisabolol / Chamomile oil
1 Carvacrol
1 D-limonene
1 Shilajit/Fulvic Acid
1 Gallic acid
1 Hibiscus sabdariffa
1 Isovitexin
1 Lycopene
1 Moringa oleifera
1 nicotinamide adenine dinucleotide
1 Rosmarinic acid
1 Selenium
1 Selenium NanoParticles
1 Silymarin (Milk Thistle) silibinin
1 Silicic Acid
1 Curcumin
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#:1251  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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