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Sildenafil attenuates renal injury in an experimental model of rat cisplatin-induced nephrotoxicity.

Author	Kang Wook Lee, Jin Young Jeong, Beom Jin Lim, Yoon-Kyung Chang, Sang-Ju Lee, Ki-Ryang Na, Young-Tai Shin, Dae Eun Choi
Citation Information	Toxicology, 257:137-43 (2009)
Keywords	Animals, Antineoplastic Agents, Blood Urea Nitrogen, Blotting, Western, Caspase 3, Cisplatin, Creatinine, In Situ Nick-End Labeling, Kidney, Kidney Diseases, Kidney Function Tests, Male, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III, Phosphodiesterase Inhibitors, Piperazines, Purines, RNA, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, Sulfones, bcl-2-Associated X Protein
Related Products	S7100
Pub Med ID	19152827

Sildenafil is the first commercially available selective inhibitor of phosphodiesterase-5 (PDE5) and is widely used for the treatment of erectile dysfunction. In recent years, investigations of the role of sildenafil in cardioprotection in animal models have received considerable interest. We evaluated whether sildenafil can attenuate cisplatin-induced nephrotoxicity in a rat experimental model. Male Sprague-Dawley rats were divided into five groups: control rats, sildenafil-control rats, cisplatin-injected rats (5 mg kg(-1) IP, single dose), sildenafil-treated cisplatin-injected rats (0.4 mg kg(-1), daily), and sildenafil+NG-nitro-l-arginine methyl ester hydrochloride (l-NAME)-treated rats. The molecular, functional, and structural parameters of the kidney were measured. At 96 h after cisplatin injection, serum levels of creatinine were lower in rats treated with both sildenafil+cisplatin compared with rats treated with cisplatin alone, and renal iNOS and eNOS expression was significantly higher in sildenafil+cisplatin-treated rats compared with rats treated with cisplatin alone (all P0.05). Renal Bax gene and protein expression was significantly higher in cisplatin-treated rats compared with control rats, and sildenafil treatment significantly reduced the levels of Bax and increased the renal Bax/Bcl-2 ratio (P0.05). Sildenafil treatment also reduced renal caspase-3 activation and TUNEL-positive apoptotic cells. These data suggest that sildenafil attenuates experimental cisplatin-induced nephrotoxicity by preventing apoptosis.