The Protective Impacts of Against Cisplatin-induced Renal Injury Through the Regulation of Oxidative Stress, Pro-inflammatory Cytokines and Bax/Bcl2

One of the main antineoplastic chemotherapy medications is , of which nephropathy is a major side effect. In this current study, we aim to investigate the molecular protective effect of () on -induced nephrotoxicity. In total, 48 healthy male albino rats were allocated into 4 groups. Group 1 received saline intraperitoneally (IP) twice per week (normal rats). Group 2 received (100 mg/kg BW orally). Group 3 were injected with cisplatin (1.5 mg/kg IP) twice per week. Group 4 received and on the 4th day received cisplatin (1.5 mg/kg IP) for 21 days. After 3 weeks of experiment, blood and renal tissues were taken for serum analysis, gene expression using qRT-polymerase chain reaction, and renal histopathology. As per our findings, it was found that significantly ameliorated the alterations in body weight, relative kidney weight, and the disturbance in examined renal markers. Furthermore, SP recovered and restored cisplatin-induced oxidative stress biomarkers (MDA and NO) and antioxidant activity (SOD and GSH) and cisplatin-induced upregulation in the gene expression of TNF-α, inducible nitric oxide synthase, TGF1-β, IL-1β, and IL-6. Interestingly, these gene expressions were ameliorated by the SP pre-administration. Furthermore, upregulated pro-apoptotic gene , whereas it downregulated anti-apoptotic gene . Interestingly, mitigated this alteration in apoptosis and anti-apoptotic associated genes. Renal histopathology revealed the protective impacts of against -induced severe glomerular congestion, hemorrhage, inflammatory cell infiltration, degeneration, and severe necrosis in renal glomeruli and tubules. In conclusion, has a protective effect against cisplatin-induced renal damage through modulating oxidative stress and anti-inflammatory, anti-necrotic, and anti-apoptotic-associated genes.