uricA Cancer Research Results

uricA, uric acid: Click to Expand ⟱

Source:

Type:

Uric acid is a bit of a double-edged sword when it comes to oxidative stress:

Antioxidant Effects:
-Uric acid is considered one of the most important antioxidants in human plasma. It can scavenge reactive oxygen species (ROS) such as singlet oxygen and peroxyl radicals.
-Its antioxidant properties help protect cells and tissues from oxidative damage, contributing to the overall antioxidant capacity of the blood.

Pro-oxidant Effects:
-Under certain conditions, especially at high concentrations, uric acid can also act as a pro-oxidant. For example, it may promote inflammation and oxidative stress in vascular tissues, which has been associated with conditions like hypertension and cardiovascular disease.
-The formation of monosodium urate crystals (as seen in gout) is linked to inflammatory reactions, and these crystals can contribute to local oxidative stress.

-Some studies have reported that elevated serum uric acid levels can be found in patients with certain cancers, possibly reflecting high cell turnover or altered metabolism. In some cases, higher local concentrations of uric acid might contribute to the antioxidant environment or even affect inflammatory processes.

Scientific Papers found: Click to Expand⟱

3170-

Ash,

Withaferin A protects against hyperuricemia induced kidney injury and its possible mechanisms

in-vitro,

Nor,

NRK52E

in-vivo,

NA,

mice

*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.

2630-

Ba,

Baicalein decreases uric acid and prevents hyperuricemic nephropathy in mice

in-vivo,

Nor,

50 mg/kg/d

mice

*RenoP↑, Thus, we concluded that baicalein executed a kidney-protection action in hyperuricemia and therefore may be used as a therapeutic alternative for hyperuricemic nephropathy.
*uricA↓, Baicalein lowered UA and protected kidney against hyperuricemia
*ROS↓, Baicalein prevented renal oxidative stress in hyperuricemia mice.
EMT↓, Baicalein inhibits hyperuricemia-induced epithelial-mesenchymal transition (EMT) process

6542-

BSB,

Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol

Review,

Var,

Review,

Park,

Review,

AD,

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↓,

7012-

Fuc,

Fucoidan: A promising natural therapeutic agent for protecting human kidney health

Review,

EC,

*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

4022-

FulvicA,

Chemo,

Shilajit potentiates the effect of chemotherapeutic drugs and mitigates metastasis induced liver and kidney damages in osteosarcoma rats

in-vivo,

OS,

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↑,

7486-

H2,

Effects of hydrogen-rich water on blood uric acid in patients with hyperuricemia: A randomized placebo-controlled trial

Trial,

Nor,

100 participants

*eff↑, The high-dose of HRW was more effective than low-dose HRW in controlling blood uric acid.
*uricA↓, significant reduction in blood uric acid levels compared to the baseline (488.2 ± 54.1 μmol/L to 446.8 ± 57.1 μmol/L, P < 0.05).
*toxicity↓, As a rather safe agent, the prolonged consumption of HRW may be feasible in the management of hyperuricemia.
*antiOx↑, Molecular hydrogen (H2) has been proven to be an anti-oxidative and anti-inflammatory agen
*Inflam↓,
*Dose↝, various routes for H2 administration such as H2-rich water (HRW) drinking, H2 gas inhalation, and H2 water bath [21,22]. HRW refers to regular water that contains dissolved H2, and HRW drinking is convenient and extremely bio-safe.
*Dose↝, The High-HRW group consumed three bottles of HRW daily.330 mL per bottle. one bottle of water within 10 min in the morning, noon, and evening, respectively.
*Dose↝, H2 concentration was ≥4.66 mg/L. By calculation, the daily H2 intake doses were about 3.08 mg and 4.61 mg in the Low-HRW group and High-HRW group, respectively.
*toxicity↓, H2 is acknowledged as a relatively safe agent. In the food industry, H2 has obtained official approval as a food additive due to its non-toxic properties
*Dose↓, The solubility of H2 in water is approximately 1.6 mg/L under standard conditions (20 °C, 101.325 kPa). The utilization of micro and nanobubbles technologies has been shown to enhance the solubility of H2 in water.
*ROS↓, The mechanisms of HRW consumption on regulating oxidative stress and inflammatory responses, and thereby reducing blood uric acid levels require further inquiry.

7785-

ISL,

Enhancement of Oral Bioavailability and Anti-hyperuricemic Activity of Isoliquiritigenin via Self-Microemulsifying Drug Delivery System

in-vivo,

Nor,

rats

*Dose↝, The ISL-loaded self-microemulsifying drug delivery system (ISL-SMEDDS) was comprised of ethyl oleate (EO, oil phase), Tween 80 (surfactant), and PEG 400 (co-surfactant).
*BioAv↑, The oral bioavailability of the ISL-SMEDDS was enhanced by 4.71 times in comparison with the free ISL solution.
*uricA↓, More importantly, ISL-SMEDDS significantly reduced uric acid level by inhibiting xanthine oxidase (XOD) activity in the model rats.
*XO↓,

3847-

MSM,

Methylsulfonylmethane: Applications and Safety of a Novel Dietary Supplement

Review,

Arthritis,

*Inflam↓, common use as an anti-inflammatory agent
*Pain↓, A variety of health-specific outcome measures are improved with MSM supplementation, including inflammation, joint/muscle pain, oxidative stress, and antioxidant capacity.
*ROS↓,
*antiOx↑,
*Dose↝, MSM is well-tolerated by most individuals at dosages of up to four grams daily, with few known and mild side effects
*Half-Life↝, Pharmacokinetic studies indicate that MSM is rapidly absorbed in rats [63,64] and humans [65], taking 2.1 h and <1 h, respectively.
*NF-kB↓, The inhibitory effect of MSM on NF-κB results in the downregulation of mRNA for interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) in vitro
*IL1↓,
*IL6↓,
*TNF-α↓,
*iNOS↓, MSM can also diminish the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) through suppression of NF-κB;
*COX2/PTGS2↓,
*NLRP3↓, MSM negatively affects the expression of the NLRP3 inflammasome by downregulating the NF-κB production of the NLRP3 inflammasome transcript and/or by blocking the activation signal in the form of mitochondrial generated reactive oxygen species (ROS)
*NRF2↑, MSM influences the activation of at least four types of transcription factors: NF-κB, signal transducers and activators of transcription (STAT), p53, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2).
*STAT↓, MSM has been shown to repress the expression or activities of STAT transcription factors in a number of cancer cell lines in vitro
*Cartilage↑, , in vitro studies suggest that MSM protects cartilage through its suppressive effects on IL-1β and TNF-α
*eff↑, Supplementation with glucosamine, chondroitin sulfate, MSM, guava leaf extract, and Vitamin D improved physical function in patients with knee osteoarthritis based on the Japanese Knee OA Measure
*eff↑, MSM in combination with boswellic acid was also shown to improve knee joint function as assessed through the Lequesne Index
*GSH↑, MSM is able to restore the reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio to normal levels, decrease NO production, and reduce neuronal ROS production following HIV-1 Tat exposure
*uricA↓, Humans studies show promise for MSM as an antioxidant with similar results noted, including reductions in MDA [19,167,168], protein carbonyls (PC) [167,168], and uric acid [168] and increases in GSH [167] and TEAC [159,161,168].
tumCV↓, MSM independently has been shown to be cytotoxic to cancer cells by inhibiting cell viability through the induction of cell cycle arrest [119,122,123], necrosis [119], or apoptosis
TumCCA↑,
necrosis↑,
Apoptosis↑,
VEGF↓, reduced expression of oncogenic proteins such as vascular endothelial growth factor (VEGF) [99,100,101,123], heat shock protein (HSP)90α [100], and insulin-like growth factor-1 receptor (IGF-1R)
HSP90↓,
IGF-1?,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1, chemoP↑, 1,
Total Targets: 43

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 2, Buty↑, 1, diuretic↑, 1, GLP-1R↑, 1, SCFAs↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 4, Catalase↑, 3, GPx↑, 1, GSH↑, 3, HO-1↑, 1, Keap1↑, 1, lipid-P↓, 2, MDA↓, 2, NRF2↑, 2, ROS↓, 5, SOD↑, 3, TBARS↓, 1, uricA↓, 7,

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1, MMP↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

BUN↓, 1, SIRT1↑, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1, Apoptosis↓, 2, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 1, Cyt‑c↓, 1, iNOS↓, 3, MAPK↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,

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

ERK↑, 1, PI3K↓, 1, STAT↓, 1, STAT3↓, 1,

Migration(tgid=13) ⓘ

Cartilage↑, 1, COL1↓, 1, Fibrosis↓, 1, MMP13↓, 1, RAGE↓, 1, TGF-β1↓, 1, TJ↑, 1, α-SMA↓, 2,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1, GastroP↑, 1, IBI↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1, COX2/PTGS2↓, 3, HMGB1↓, 1, IL1↓, 1, IL1β↓, 1, IL6↓, 2, IL6↑, 1, Imm↑, 1, Inflam↓, 4, JAK2↓, 1, NF-kB↓, 2, TNF-α↓, 3,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1, BChE↓, 1,

Protein Aggregation(tgid=19) ⓘ

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

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 4, Dose↓, 1, Dose↝, 6, eff↑, 4, Half-Life↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1, creat↓, 2, GutMicro↑, 1, IL6↓, 2, IL6↑, 1, RAGE↓, 1,

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2, hepatoP↑, 1, motorD↑, 1, neuroP↑, 1, Pain↓, 2, RenoP↑, 4, toxicity↓, 3,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1, CD8+↑, 1,
Total Targets: 85

Scientific Paper Hit Count for: uricA, uric acid

1 Ashwagandha(Withaferin A)
1 Baicalein
1 α-Bisabolol / Chamomile oil
1 Fucoidan
1 Shilajit/Fulvic Acid
1 Chemotherapy
1 Hydrogen Gas
1 Isoliquiritigenin
1 Methylsulfonylmethane

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#:1322  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

uricA Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

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

Migration(tgid=13) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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