Yuan Chen1, Yan-Yan Tao, Feng-Hua Li. 1. Institute of Liver Diseases, Shuguang Hospital, Shanghai University of TCM, Shanghai.
Abstract
OBJECTIVE: To observe the effects of Danggui Buxue Decoction (DBD) on liver fibrosis and to explore its mechanism related to hepatic lipid peroxidation in rats. METHODS: Liver fibrosis model was established in 28 rats by the combination of injecting carbon tetrachloride (CCl4) subcutaneously and feeding high lipid and low protein diet. The model rats were randomly divided into 2 groups, the model group (n = 14) and the treated group (n = 14). Besides, a normal group was set up with 10 normal rats. For the treated group, rats were administered with DBD at a dosage of 6 g/kg body weight once a day by gastrogavage starting from the day of modeling for 6 successive weeks and to the control group, equal volume of normal saline was administered instead. The inflammation and fatty degeneration in rat liver tissues were examined with HE staining; the collagen deposition observed with sirius red; the liver function including serum level of alanine transaminase (ALT), aspartate aminotransferase (AST), albumin (Alb) and total bilirubin (TBil) were determined using corresponding test kits; the hepatic lipid peroxidation indexes, including triglyceride (TG), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by biochemical methods; the hepatic hydroxyproline (Hyp) content was detected with Jamall's method and the expression of collagen type I was analyzed by Western blotting. RESULTS: Compared with those in the normal rats, serum ALT, AST, TBil level, TG and MDA content remarkablely increased, level of Alb and SOD activity decreased, and hepatic fatty degeneration and collagen pathological deposition in liver was more obvious in the model rats (all P < 0.05). While in the DBD group, the hepatic fatty degeneration and collagen deposition were significantly improved, changes of all the above-mentioned indexes were significantly reversed (P <0.05). CONCLUSION: DBD has a good antagonist effect against experimental liver fibrosis, and its mechanism may be related to the anti-lipid peroxidation injury effect.
OBJECTIVE: To observe the effects of Danggui Buxue Decoction (DBD) on liver fibrosis and to explore its mechanism related to hepatic lipid peroxidation in rats. METHODS:Liver fibrosis model was established in 28 rats by the combination of injecting carbon tetrachloride (CCl4) subcutaneously and feeding high lipid and low protein diet. The model rats were randomly divided into 2 groups, the model group (n = 14) and the treated group (n = 14). Besides, a normal group was set up with 10 normal rats. For the treated group, rats were administered with DBD at a dosage of 6 g/kg body weight once a day by gastrogavage starting from the day of modeling for 6 successive weeks and to the control group, equal volume of normal saline was administered instead. The inflammation and fatty degeneration in rat liver tissues were examined with HE staining; the collagen deposition observed with sirius red; the liver function including serum level of alanine transaminase (ALT), aspartate aminotransferase (AST), albumin (Alb) and total bilirubin (TBil) were determined using corresponding test kits; the hepatic lipid peroxidation indexes, including triglyceride (TG), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by biochemical methods; the hepatic hydroxyproline (Hyp) content was detected with Jamall's method and the expression of collagen type I was analyzed by Western blotting. RESULTS: Compared with those in the normal rats, serum ALT, AST, TBil level, TG and MDA content remarkablely increased, level of Alb and SOD activity decreased, and hepatic fatty degeneration and collagen pathological deposition in liver was more obvious in the model rats (all P < 0.05). While in the DBD group, the hepatic fatty degeneration and collagen deposition were significantly improved, changes of all the above-mentioned indexes were significantly reversed (P <0.05). CONCLUSION: DBD has a good antagonist effect against experimental liver fibrosis, and its mechanism may be related to the anti-lipid peroxidation injury effect.