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-α, 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.