ORIGINAL PAPER Protection against cisplatin-induced nephrotoxicity in mice by Curcuma comosa Roxb. ethanol extract Surawat Jariyawat Æ Pranida Kigpituck Æ Kanoknetr Suksen Æ Aporn Chuncharunee Æ Arusa Chaovanalikit Æ Pawinee Piyachaturawat Received: 13 January 2009 / Accepted: 25 May 2009 / Published online: 18 June 2009 Ó The Japanese Society of Pharmacognosy and Springer 2009 Abstract The protective effect of an ethanol extract of Curcuma comosa against cisplatin-induced renal toxicity in mice was studied. Adult male mice were pretreated for 4 days with the ethanol extract of C. comosa [100–200 mg/ kg body weight (BW), orally (p.o.)] before injection of cisplatin (12.5 mg/kg BW, intraperitoneally (i.p.)). Five days later the mice were killed, and blood samples were collected to determine blood urea nitrogen (BUN) and plasma creatinine levels. Kidneys were examined histopa- thologically and levels of lipid peroxidation, gluthathione (GSH) content, and superoxide dismutase (SOD), glutha- thione peroxidase (GPx), and catalase (CAT) activities were determined. Histological examinations revealed degenerative changes and tubular necrosis in mice treated with cisplatin, which were improved by pretreatment with C. comosa ethanol extract. Cisplatin raised BUN, creati- nine, and kidney lipid peroxidation levels, and lowered kidney GSH content and levels of GPx, SOD, and CAT activities, all of which (except SOD and CAT) could be restored to normal values by pretreatment with 200 mg/kg BW of C. comosa ethanol extract. In addition, the ethanol extract of C. comosa and its isolated diarylheptanoid compound also exhibited radical scavenging activities. The results suggest that the ethanol extract of C. comosa exhibits effective protection against cisplatin-induced nephrotoxicity mediated through its antioxidant activity. Keywords Curcuma comosa Á Antioxidant activity Á Cisplatin Á Nephroprotection Introduction Cisplatin, cis-diaminedichloroplatinum(II), is one of the most widely used chemotherapeutic agents for the treat- ment of a variety of malignancies and solid tumors [1]. Although the therapeutic effects of cisplatin are improved by dose escalation, high-dose therapy is limited by its cumulative nephrotoxicity [2]. Reports of accidental overdose leading to renal failure indicate that cisplatin is sufficiently potent to be toxic to human [3]. The mechanism of cisplatin-induced nephrotoxicity is not fully understood, but inflammation and oxidative stress have been reported in cisplatin-induced nephrotoxicity [4, 5]. Upon cisplatin administration glutathione (GSH) con- tent and activities of superoxide dismutase (SOD), gluta- thione peroxidase (GPx), and catalase (CAT) are decreased [5]. A number of anti-inflammatory and antioxidant agents, such as curcumin, vitamin C, and vitamin E, provide pro- tective effects against cisplatin-induced nephrotoxicity [5, 6]. Curcumin attenuates cisplatin-induced nephrotoxicity by reducing tumor necrosis factor-alpha (TNF-a) and lipid peroxidation and by enhancing the antioxidant enzyme profile [6]. S. Jariyawat Á P. Kigpituck Á K. Suksen Á P. Piyachaturawat (&) Department of Physiology, Faculty of Science, Mahidol University, Rama 6 Road, Rachatewee, Bangkok 10400, Thailand e-mail: scppy@mahidol.ac.th P. Kigpituck Á P. Piyachaturawat Graduate Program in Toxicology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand A. Chuncharunee Department of Anatomy, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand A. Chaovanalikit Department of Home Economics, Faculty of Science, Srinakharinwirot University, Bangkok 10110, Thailand 123 J Nat Med (2009) 63:430–436 DOI 10.1007/s11418-009-0345-5