Cisplatin (CIS) is an antineoplastic agent used for treating solid organ tumors. Toxic side effects of CIS treatment include nephrotoxicity, neurotoxicity, ototoxicity, myelosuppression and hepatotoxicity. Dexpanthenol (DEX) exhibits antioxidant and anti-inflammatory effects and protective effects against free oxygen radicals. We investigated the protective effects of DEX on CIS induced nephrotoxicity. Animals were divided into four groups of 10. The control group was given saline. The DEX group was treated with DEX for 10 days. The CIS group was treated with a single dose of CIS. The DEX + CIS group was given a single dose of CIS followed by DEX for 10 days. We found increased levels of malondialdehyde (MDA), blood urea nitrogen (BUN) and creatinine, while superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and myeloperoxidase (MPO) levels were decreased in the CIS group. MDA, BUN and creatinine levels were decreased, while SOD, CAT, GPx and MPO levels were increased in the DEX + CIS group. Renal tubule damage, inflammation and histopathology scores were significantly higher in the CIS group than the control. The DEX + CIS group exhibited less renal tubule damage and inflammation, and lower histopathological assessment scores than the CIS group. Significant cortical tubule damage and interstitial inflammation were observed in the CIS group. Tubule damage was slightly less, and mild tubule dilation and less cast formation were observed in the DEX + CIS group; also, inflammation was less severe than for the CIS group. DEX may have therapeutic potential for treating CIS induced nephrotoxicity due to its antioxidant and anti-inflammatory properties.