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Updated: Jan 13, 2026
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
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Oxyresveratrol Protects Against Cisplatin Nephrotoxicity in Rats Through TXNIP-Mediated NLRP3/Caspase-1/IL-1β
Nagihan Demirtas1, Zekai Halici2, Elham Bahador Zirh3
1Department of Pharmaceutical Toxicology, Faculty of Pharmacy, Atatürk University, Erzurum, Turkey.
Journal of Biochemical and Molecular Toxicology
|January 8, 2026
Summary
Oxyresveratrol (OXY) mitigates cisplatin-induced nephrotoxicity by reducing endoplasmic reticulum stress (ERS) and NLRP3 inflammasome activation. This antioxidant compound shows potential in protecting kidney function against drug-induced damage.
Area of Science:
- Nephrology
- Toxicology
- Molecular Biology
Background:
- Cisplatin (CIS) is a widely used chemotherapy agent with significant nephrotoxic side effects.
- Endoplasmic reticulum stress (ERS) and NLRP3 inflammasome activation are implicated in CIS-induced kidney damage.
- Oxyresveratrol (OXY) is a natural polyphenol with known antioxidant properties.
Purpose of the Study:
- To investigate the protective effects of OXY against CIS-induced nephrotoxicity.
- To elucidate the role of ERS-mediated NLRP3 inflammasome activity in this process.
- To evaluate OXY's impact on kidney function, oxidative stress, and molecular markers.
Main Methods:
- Rats were administered CIS to induce nephrotoxicity.
- OXY was administered orally at varying doses (5, 10, 20 mg/kg).
- Kidney function, oxidative stress markers (SOD, GSH, MDA), and molecular parameters of ERS and NLRP3 inflammasome were assessed.
Main Results:
- CIS administration significantly increased ERS markers and NLRP3 inflammasome activity in renal tissue.
- CIS-induced nephrotoxicity was associated with increased oxidative stress (decreased SOD and GSH, increased MDA).
- OXY treatment dose-dependently reduced serum urea and creatinine levels, improved oxidative stress markers, and decreased ERS molecular parameters.
Conclusions:
- CIS-induced nephrotoxicity involves ERS-mediated NLRP3 inflammasome activation.
- OXY demonstrates significant protective effects against CIS-induced kidney damage.
- OXY's antioxidant properties may mediate its renoprotective effects by targeting ERS and NLRP3 inflammasome pathways.
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