Raloxifene impedes cisplatin-induced nephrotoxicity through inhibition of Proinflammatory cytokines in female wistar rats

Cisplatin mediated nephrotoxicity is the main obstacle in the practice of cisplatin as a chemotherapeutic agent. Conversely, it continues to be the most commonly used anticancer agent to treat several solid tumours. This study investigated the effect of raloxifene pretreatment on nephrotoxicity mediated by cisplatin in an experimental animal model. The levels of blood urea nitrogen, creatinine, and albumin were measured to evaluate the renal damage, and the levels of proinflammatory cytokines such as interleukin 6 (IL-6), interleukin 10 (IL-10), and tumour necrosis factor alpha (TNF-alpha) were measured to assess the systemic inflammation. Cisplatin in a single dose of 7.5mg/kg showed a substantial rise in serum levels of blood urea nitrogen, creatinine along with TNF-alpha and IL-6 and, fall in albumin and IL 10 levels. Nevertheless, there was no substantial change in a group treated with raloxifene 7.5mg/kg. We observed a substantial fall in the levels of blood urea nitrogen, creatinine along with TNF-alpha and IL-6 and a rise in albumin and IL 10 levels. The current study established a protective effect of raloxifene in cisplatin mediated nephrotoxicity and this is due to its potential anti-oxidant and anti-inflammatory properties. Therefore, a cisplatin induced nephrotoxicity can be prevented by the use of raloxifene as a therapeutic adjuvant.