Oxyresveratrol Protects Against Cisplatin Nephrotoxicity in Rats Through TXNIP‐Mediated NLRP3/Caspase‐1/IL‐1β Pathway: Regulating Endoplasmic Reticulum Stress

The aim of this study was to investigate the effects of oxyresveratrol (OXY) on CIS-induced nephrotoxicity through endoplasmic reticulum stress (ERS)-mediated NLRP3 inflammasome activity. A total of 36 rats were randomly divided into six groups (n = 6). Nephrotoxicity was induced by a single intraperitoneal (i.p.) injection of CIS (10 mg/kg) on day 1 in the experimental groups. OXY was administered orally at doses of 5, 10, and 20 mg/kg for three consecutive days in the treatment groups. Kidney function tests, oxidative stress markers, and molecular parameters were evaluated. Molecular analysis revealed a significant upregulation of mRNA expression of ER stress-mediated markers associated with increased NLRP3 inflammasome activity in renal tissue following CIS induced toxicity. Furthermore, oxidative stress was determined with significantly decreased SOD activity and GSH levels and increased MDA levels with cisplatin administration. It has been shown that OXY administration at increasing doses causes a decrease in serum urea and creatinine levels and changes in oxidative stress parameters, and also it was shown to cause a decrease in molecular parameters of ER stress. New findings have revealed that ER stress-mediated NLRP3 activation is induced in the kidneys due to cisplatin toxicity and that OXY, a potent antioxidant, may be effective through the pathways that are specified in cisplatin nephrotoxicity.