uricA Cancer Research Results

uricA, uric acid: Click to Expand ⟱
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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, 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.

2630- Ba,    Baicalein decreases uric acid and prevents hyperuricemic nephropathy in mice
- in-vivo, Nor, NA
*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, 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↓,
*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↓, 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↓,
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↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,

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↑,

3847- MSM,    Methylsulfonylmethane: Applications and Safety of a Novel Dietary Supplement
- Review, Arthritis, NA
*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↓,
*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 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Bil↝, 1,   uricA↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Bak↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   BID↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Fas↑, 1,   necrosis↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP90↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 2,  

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

EMT↓, 1,   FGF↓, 1,   IGF-1?, 1,  

Migration(tgid=13) ⓘ

CEA↓, 1,   TIMP2↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↑, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   NF-kB↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   RadioS↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

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

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

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

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

BUN↓, 1,  

Cell Death(tgid=5) ⓘ

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

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

STAT↓, 1,  

Migration(tgid=13) ⓘ

Cartilage↑, 1,   MMP13↓, 1,   α-SMA↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GastroP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2↓, 3,   IL1↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL6↑, 1,   Imm↑, 1,   Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BChE↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

creat↓, 2,   IL6↓, 2,   IL6↑, 1,  

Functional Outcomes(tgid=23) ⓘ

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

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   CD8+↑, 1,  
Total Targets: 58

Scientific Paper Hit Count for: uricA, uric acid
1 Ashwagandha(Withaferin A)
1 Baicalein
1 α-Bisabolol / Chamomile oil
1 Shilajit/Fulvic Acid
1 Chemotherapy
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

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