Icaritin delays CCl4-induced hepatic cirrhosis in rats by protecting hepatocytes from oxidative injury
10.3724/SP.J.1008.2011.00625
- Author:
Hai-Hua QIAN
1
Author Information
1. Department of Molecular Oncology
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Icaritin;
Liverfibrosis;
Liverinjury
- From:
Academic Journal of Second Military Medical University
2011;32(6):625-629
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of icaritin in delaying the progression of liver cirrhotic process in rats and the related mechanism. Methods For invitro study, primary rat hepatocytes were obtained by perfusing the liver of male Wistar rats; the cultured cells we reexposed to the fresh medium containing CCl4, and then treated with various concentrations of icaritin. The activities of alanine transaninase(ALT) and glutamic-oxaloacetic transaminase(AST) inculture medium were measured with an automatic biochemical analyzer. The intracellular contents of malondialdehyde (MDA) and superoxide dismutase(SOD) were determined by spectro-photometry; the apoptotic cells were detected by the TUNEL method. Forin vivostudy, CCl4-induced experimental rat hepatic fibrosis model was established and was treated with icaritin. Serum levels of ALT, AST, albumin(ALB), andglobulin(GLB) were measured; the pathological changes and collagen-expression in livers were observed by HE staining and immunohistochemistry, respectively. Results CCl4 significantly increased the activities of ALT, AST, and the contents of MDA in culture media of hepatocytes, and significantly decreased the SOD activity. More apoptotic cells were observed in CCl4 group than that in icaritin group. The ALT, AST activities in culture supernatant and the intracellular MDA contents in icaritin group were significantly lower than those in both model group and drug carrier group, while intracellular SOD activity was much higher than that in other two groups(P<0.05). Icaritin also reduced the apoptotic ratios of hepatocytes induced by CCl4 compared with model group(P<0.05 or 0.01). In the in vivo experiment, icaritin treatment significantly reduced serum levels of ALT and AST compared with model group(P<0.05) and greatly improved CCl4-induced liver histopathological injuries and collagen I deposition in the liver tissues. Conclusion Icaritin treatment can attenuate CCl4-induced cirrhosis in rats, atleast in part, by protecting the hepatocytes from peroxidation product.
