| Introduction:Cisplatin (Cis-diamminedichloroplatinum, CDDP) is an anticancer medicine that has been widely used currently. It is recommened as the primary chemotherapeutic agent in the treatment of 18 kinds of cancer including those of the head, neck, testis and ovary, by American and Canada. In the treatment of other cancer, it is also used as the secondary chemotherapeutic agent. Among many chemotherapeutic regimens in our country, CDDP is also considered the primary agent. Even though it is effective as an anticancer medicine, unfortunately it has been found that there are many side effects with this medicine, such as the ototoxicity, bone marrow suppression, hepatotoxicity, and especially nephrotoxicity. At present, there is much more interest exerted in probing the mechanisms of cisplatin-induced nephrotoxicity and developing new methods to ameliorate renal damage. Despite the underlying mechanism of cisplatin-induced nephrotoxicity is still not well known,many recent shudies indicate that the oxidative stress is closely related to the nephrotoxicity induced by cisplatin; another possible mechanism involves CDDP binding to nitrogen atoms of DNA base and forming a stable Pt-DNA adducts, which is subsequently forming an interstrand cross-link with double-strand DNA. Curcumin is a phenolic compound , that is derived from the rhizome of the herb turmeric (Curcumalonga L.). it has many pharmacologic activity such as anti-tumor, anti-oxidative and anti-inflammatory et al with low toxicity. In vivo, Curcumin can remarkably inhibit the growth of skin cancer, forestomach cancer, colon cancer and breast cancer et al. In recent reports, it is that curcumin could induced the apoptosis in many cultured tumor cells such as MGC803,Bel7402,Bf16,K562/ADM. According to the early investigation, it has been suggested that CMN is the inhibitor of phospholipid proxidative action by iron-catalysis in the microsome of liver in rats. The anti-oxidative effects of CMN is much better than that of α-T. however, CMN could also inhibit the forming of DNA-adducts, reduceing the content and change the dactylogram diagram of DNA-adducts and thus protecting the marcromoleculars in the cells such as DNA.In this stady, we had investigated the mechanisms of CDDP-induced nephrotoxicity from the aspects of oxidative stress and DNA damage in vitro and in vivo. we also investigated the influence of CMN on CDDP-induced nephrotoxicity in rats and attempted to explore its possible mechanisms and widen the clinical utilization of CDDP and CMN.Methods:In vivo, female Sprague-Dawley rats were randomly divided into six groups according to their weights (seven rats in each). Each group was treated as the follows: ⑴Control: animals were received an equal volume of saline by gavage(ig) as that of the CMN group for 3 days, and after 1h of the second gavage animals were treatment of an equal volume of saline as that of the CDDP group by injection of the abdomen (ip); ⑵CMN: animals were received 80mg/kg CMN by ig for 3 days, and after 1h of the second gavage animals were treatment of an equal volume of saline as that of the CDDP group by injection of the abdomen (ip); ⑶ CDDP (ip5.5 mg/kg CDDP): animals were received an equal volume of saline by gavage(ig) as that of the CMN group for 3 days, and after 1h of the second gavage animals were treatment of 5.5 mg/kg CDDP by injection of the abdomen (ip);⑷CDDP+20 mg/kg CMN: animals were received 20mg/kg CMN by ig for 3 days, and after 1h of the second gavage animals were treatment of 5.5 mg/kg CDDP by injection of the abdomen (ip);⑸CDDP+40 mg/kg CMN: animals were received 40mg/kg CMN and the treatment was the same as that of the group ⑷; ⑹CDDP+80 mg/kg CMN: animals were received 80mg/kg CMN and the treatment was the same as that of the group ⑷. Blood samples were collected on Day 1,3,5 after the CDDP treatment. After CDDP treatment on Day 5 the rats were killed. Kidney samples were collected. Nephrotoxicity was assessed by the measurements of body weight, kidney index, contents of bloo...
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