复方绞芪方对非酒精性脂肪性肝炎大鼠肝组织SCD-1表达的影响

Effect of Fufang Jiaoqi Fang on Expression of SCD-1 in Liver Tissue of Rats with Non-Alcoholic Steatohepatitis

目的:观察复方绞芪方对高脂高糖饮食诱导的非酒精性脂肪性肝炎(NASH)大鼠肝组织SCD-1表达的影响,探讨其防治NASH的作用机理。方法:以高脂高糖饮食喂养SD大鼠12周建立NASH模型,以不同剂量的复方绞芪方进行干预,测定大鼠血清ALT、AST、FFA含量和肝组织匀浆TG、CHOL含量变化、常规HE染色观察肝组织的病理改变并计算NAFLD活动度积分(NAS);用免疫组织化学法检测肝组织SCD-1的表达。结果:模型组大鼠的血清ALT、AST、FFA水平以及肝组织中的CHOL、TG含量较正常组明显增加,肝组织NAS计分明显升高,SCD-1蛋白表达明显下降。应用复方绞芪方进行干预后,大鼠的NAS计分较模型组显著降低,肝功能明显改善,血清FFA水平明显下降同时肝组织中CHOL和TG含量也明显下降,肝组织中SCD-1蛋白表达明显增加。结论:高脂高糖饮食诱导的NASH大鼠存在脂肪酸代谢酶的紊乱;复方绞芪方通过调节脂肪酸代谢酶的活性,增加SCD-1的表达,减少脂质在肝脏聚集及相关的肝功能损害,这可能是其防治NASH的作用机制之一。

Objective ：To investigate the method of Fufang Jiaoqi Fang on the expression of SCD - 1 in liver tissue of rats with non - alcoholic steatohepatitis. Method： The non - alcoholic steatohepatitis model was induced by high fat and sugar diet to SD rats for twelve weeks and treated by different doses of Fufang Jiaoqi Fang. Determination of serum ALT, AST and FFA contents and liver tissue TG and CHOL contents was carried out. The pathological changes of liver tissue were observed with HE staining to calculate NAFLD activity score and the SCD - 1 protein quantity was measured by Im- munohistochemistry. Result： In model group, serum ALT, AST and FFA levels and liver tissue CHOL and TG levels were significantly increased and the NAFLD activity scores of rats were significantly higher and SCD - 1 protein quantity ex- pressions of liver tissues were significantly decreased compared with the normal levels. The NAFLD activity score, serum ALT, AST and FFA levels and liver tissue CHOL and TG levels in Chinese medicine compound groups were all improved than that of model and SCD - 1 protein quantity expression of liver tissues was significantly increased compared with that of the model. Conclusion： High fat and sugar diet - induced NASH has fatty acid metabolism enzymes disorder. Fufang Jiaoqi Fang can be the prevention and treatment of NASH by regulating the activity of fatty acid metabolic enzymes, in- creasing the SCD - 1 protein quantity expression of liver tissues and reducing lipid accumulation in the liver and associat- ed liver dysfunction, which may be one of the mechanisms.