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目的:观察博落回提取物(Macleaya cordata extract,MCE)对实验性肝纤维化的防治作用。方法:采用CCl4复合因素诱导的大鼠肝纤维化和小鼠血吸虫肝纤维化2种模型,观测MCE干预后肝指数、肝功能生化指标[丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)]、血清纤维化指标[Ⅲ型前胶原(PCⅢ)、层黏连蛋白(LN)、透明质酸(HA))、脂质过氧化指标[谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、超氧化物歧化酶(SOD)),肝组织Ⅰ型胶原(CoⅠ)、Ⅲ型胶原(CoⅢ)及羟脯氨酸(Hyp)表达的变化,并做肝脏病理学检查。结果:在CCl4肝纤维化大鼠模型中,MCE各剂量预防组肝指数,AST含量及CoⅠ表达明显降低,高剂量预防组LN及CoⅢ表达明显降低;中剂量预防组MDA含量及CoⅢ表达明显降低;MCE治疗组肝指数、HA,MDA含量及CoⅢ表达明显降低;经MCE防治后大鼠肝纤维化程度有不同程度减轻。在小鼠血吸虫肝纤维化模型中,MCE预防组小鼠Hyp及CoⅠ表达明显降低;高剂量治疗组小鼠肝指数、PCⅢ,LN,HA,AST,ALT含量及CoⅠ表达显著降低,中剂量治疗组PCⅢ,HA,AST,ALT含量明显降低;MCE治疗给药能明显改善模型小鼠肝脏病变。结论:MCE对实验性肝纤维化有一定的防治作用,其机制可能与其保护肝细胞膜、减轻肝脏炎症及抗脂质过氧化作用有关。
Objective: To observe the preventive and therapeutic effects of macleaya cordata extract (MCE) on experimental liver fibrosis. Methods: Two models of hepatic fibrosis induced by compound CCl4 and liver fibrosis induced by schistosoma japonicum were established. The indexes of hepatic function, liver function and ALT, aspartate aminotransferase (ALT) AST), serum fibrosis indicators (PC Ⅲ, laminin and hyaluronic acid), lipid peroxidation (glutathione peroxidase (GSH- Px, MDA, SOD, Co Ⅰ, Co Ⅲ and Hyp in liver tissue were detected by Western blotting and the liver Pathological examination. Results: In the CCl4 hepatic fibrosis rat models, the liver index, AST content and Co Ⅰ expression were significantly decreased in the MCE preventive groups, while the levels of LN and Co Ⅲ in the high-dose prophylaxis group were significantly decreased. The MDA content and Co Ⅲ expression in the middle-dose prophylaxis group were significantly decreased ; MCE treatment group liver index, HA, MDA content and Co Ⅲ expression was significantly reduced; after MCE prevention and treatment of rat liver fibrosis degree to varying degrees. In mice model of schistosomal liver fibrosis, the expression of Hyp and Co Ⅰ in MCE prevention group was significantly decreased; the content of liver fibrosis index, PC Ⅲ, LN, HA, AST, ALT and Co Ⅰ in high dose group were significantly decreased, Group PCⅢ, HA, AST, ALT levels were significantly reduced; MCE treatment can significantly improve the model mice liver disease. Conclusion: MCE may play a role in prevention and treatment of experimental liver fibrosis. The mechanism may be related to the protection of liver cell membrane, alleviation of liver inflammation and anti-lipid peroxidation.