2009 Kyung Hee University Press 292 Oriental Pharmacy and Experimental Medicine 2009 9(4), 292-302 www.opem.org OPEM Hesperidin improves warm ischemia/reperfusion-induced oxidative renal injury in rats Chintan Gandhi, Rishit Zalawadia and R Balaraman* Pharmacy Department, Faculty of Technology and Engineering, M. S. University of Baroda, Kalabhavan, Baroda-390001, Gujarat, India Received for publication April 07, 2008; accepted March 20, 2009 SUMMARY Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies showed that antioxidant treatments attenuated renal ischemia/reperfusion injury. The objective of this study was to examine the role of hesperidin in modulating reactive oxygen species induced inflammation and apoptosis after renal ischemia/reperfusion injury. Rats were subjected to right nephrectomy, 15 days later 45 min of renal ischemia and 24 h reperfusion with or without treatment with hesperidin. Renal function, inflammation and apoptosis were compared at 24 h after reperfusion injury. Hesperidin improved the renal dysfunction and reduced inflammation and apoptosis after ischemia/reperfusion injury. In conclusion, hesperidin shows potent anti-apoptotic and anti- inflammatory properties due to antioxidant property. These findings may have major implications in the treatment of human ischemic acute renal failure. Key words: Antioxidant; Hesperidin; Ischemia reperfusion injury; Renal ischemia INTRODUCTION Postoperative acute renal failure in consequence of ischemia and reperfusion (I/R) injury can occur after kidney transplantation (Bouchier-Hayes et al. , 1999). Ischemic cell injury in the kidney occurs during cardiovascular surgery, renal transplantation as well as the early allograft rejection subsequent to renal transplantation (Manuela, 2003). Excessive reactive oxygen species (ROS) generation occurs in I/R is proved in many biochemical and immunohis- tochemical studies. Generation of ROS, leading to dysfunction, injury, and renal cell necrosis (Chatterjee et al. , 2000; Prabal and Chatterjee, 2007). Defense against free radical injury is provided by enzymatic (catalase, superoxide dismutase and glutathione peroxidase) and non-enzymatic (alpha tocopherol, vitamin C, allopurinol, dimethyl sulphoxide.) free radical scavengers (Mark et al. , 1991; Devinder and Kanwaljit, 2004b). The protection provided by these free radical scavengers against ROS produced during injury further supports the hypothesis, ROS are involved in the cellular pathogenesis of I/R injury. Thus, research efforts designed to prevent or ameliorate tissue injury have centered on inhibiting free radical generation during I/R injury. *Correspondence: R Balaraman, Pharmacy Department, Faculty of Technology and Engineering, M. S. University of Baroda, Kalabhavan, Baroda-390001, Gujarat, India. Tel: +02652434187; Fax: +02652418927; E-mail: rbalaraman2000 @yahoo.com DOI 10.3742/OPEM.2009.9.4.292