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However, the role of H<jats:sub>2<\/jats:sub>S in cisplatin nephrotoxicity is still debatable. Here we investigated the effect of GYY4137, a novel slow-releasing H<jats:sub>2<\/jats:sub>S donor, on cisplatin nephrotoxicity in mice. Male C57BL\/6 mice were pretreated with GYY4137 for 72\u2009h prior to cisplatin injection. After cisplatin treatment for 72\u2009h, mice developed obvious renal dysfunction and kidney injury as evidenced by elevated blood urea nitrogen (BUN) and histological damage. Consistently, these mice also showed increased proinflammatory cytokines such as TNF-<jats:italic>\u03b1<\/jats:italic>, IL-6, and IL-1<jats:italic>\u03b2<\/jats:italic>in circulation and\/or kidney tissues. Meanwhile, circulating thiobarbituric aid-reactive substances (TBARS) and renal apoptotic indices including caspase-3, Bak, and Bax were all elevated. However, application of GYY4137 further aggravated renal dysfunction and kidney structural injury in line with promoted inflammation, oxidative stress, and apoptotic response following cisplatin treatment. Taken together, our results suggested that GYY4137 exacerbated cisplatin-induced nephrotoxicity in mice possibly through promoting inflammation, oxidative stress, and apoptotic response.<\/jats:p>","DOI":"10.1155\/2016\/8145785","type":"journal-article","created":{"date-parts":[[2016,5,31]],"date-time":"2016-05-31T21:04:05Z","timestamp":1464728645000},"page":"1-10","source":"Crossref","is-referenced-by-count":26,"title":["A H<sub>2<\/sub>S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice"],"prefix":"10.1155","volume":"2016","author":[{"given":"Mi","family":"Liu","sequence":"first","affiliation":[{"name":"Institute of Hypertension, Sun Yat-Sen University School of Medicine, No. 74 Zhongshan 2nd Road, Science and Technology Building, 6th Floor, Guangzhou 510080, China"},{"name":"Department of Medicine and Veterans Affairs Medical Center, University of Utah, Salt Lake City, UT 84132, 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