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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 observe the effects of compound strangulation on the expression of SCD-1 in the liver tissue of nonalcoholic steatohepatitis (NASH) rats induced by high fat and high carbohydrate diet and to explore the mechanism of its prevention and treatment of NASH. Methods: NASH model was established by feeding high fat and high sucrose diet to SD rats for 12 weeks. The interventions of different doses of compound stilbene were performed. The levels of ALT, AST and FFA in serum and TG and CHOL contents in liver homogenates were determined. Routine HE staining was used to observe the pathological changes of liver tissue and calculate NAFLD activity score (NAS); immunohistochemistry was used to detect the expression of SCD-1 in liver tissue. Results: Serum levels of ALT, AST, FFA and CHOL, TG in liver tissue of rats in the model group were significantly higher than those in the normal group. The score of NAS in liver tissue was significantly increased and the expression of SCD-1 protein was significantly decreased. Compared with the model group, the NAS score of the rats was obviously decreased, the serum FFA level decreased significantly, and the levels of CHOL and TG in the liver tissue also decreased significantly. The SCD-1 protein The expression increased significantly. CONCLUSION: NASH rats induced by high-fat and high-sugar diet have disorder of fatty acid metabolism enzyme. Compound strangulation prescription can reduce the lipid accumulation in liver and related liver damage by regulating the activity of fatty acid metabolism enzyme, increasing the expression of SCD-1 , Which may be one of the mechanisms of its prevention and treatment of NASH.