RESUMO
Aim of the work: captopril protects against cisplatin induced nephrotoxicitity; however its potential modulatory effect on hemeoxygenase [HO]-1, antioxidants, as well as inflammatory and apoptotic markers has not yet been verified
Materials and methods: Male Sprague-Dawley rats were divided into control [saline], cisplatin [5 mg/kg; i.p], and captopril [60 and 100 mg/kg] given 5 days before and after cisplatin [5 mg/kg; i.p] treatment
Results: Five-day pre- and post-treatment with captopril [60 and 100 mg/kg; i.p], for a total of 10 days, dose dependently, reduced blood urea nitrogen, as well as serum creatinine and gamma glutamyl transferase, but serum albumin and total protein levels were increased. Captopril restored renal pro-oxidant/antioxidant balance by activating glutathione peroxidase, catalase and superoxide dismutase, and boosting the renal glutathione content. These effects were accompanied by the reduction in serum and/or renal HO-1, tumor necrosis factor-alpha, monocyte chemoattractant protein-1, nitric oxide, endothelin-1 and caspase-3. Microscopically, captopril especially at 100 mg/kg dose level, prevented cisplatin-induced degenerative changes and inflammatory cell infiltration in the kidney
Conclusion: captopril protects against cisplatin nephrotoxicity by its antioxidant, anti-inflammatory and antiapoptotic potentials