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目的:基于肝脏脂肪合成和氧化环节,探讨红景天苷防治非酒精性脂肪肝的作用机制。方法:采用单纯高脂饮食14周诱导的大鼠非酒精性脂肪肝模型。在造模第9周起,随机分为模型组、红景天苷组和罗格列酮对照组,灌胃给药6周。观察肝组织病理变化;肝组织甘油三酯(TG)、游离脂肪酸(FFA)含量的变化;肝组织乙酰辅酶A羧化酶(ACCase)、丙二酰辅酶A(Malonyl Co A)、脂肪酸合成酶(FAS)、肉毒碱棕榈酰转移酶-1(CPT-1)含量的变化;肝组织ACCase和CPT-1 m RNA水平的变化。结果:模型组肝组织出现显著的肝细胞脂肪变性及空泡样变,肝组织TG、FFA、ACCase、FAS、Malonyl Co A含量和ACCase m RNA水平较正常组均显著升高(P<0.01),CPT-1含量和m RNA水平较正常组显著降低(P<0.01)。红景天苷组的上述病理改变显著减轻,肝组织TG、FFA、ACCase、Malonyl Co A、FAS含量和ACCase m RNA水平显著低于模型组(P<0.01),CPT-1含量和m RNA水平显著高于模型组(P<0.01)。结论:红景天苷能抑制肝脏脂肪合成,促进脂肪酸氧化,这可能是其防治非酒精性脂肪肝的重要机制。
OBJECTIVE: To investigate the mechanism of salidroside in preventing and treating non-alcoholic fatty liver based on liver fat synthesis and oxidation. Methods: A rat model of non-alcoholic fatty liver induced by simple high-fat diet for 14 weeks was used. From the 9th week of model establishment, the rats were randomly divided into model group, salidroside group and rosiglitazone control group, which were given intragastrically for 6 weeks. The changes of hepatic tissue pathological changes, the content of triglyceride (TG) and free fatty acid (FFA) in liver tissue were observed. The changes of hepatic acetyltransferase A carboxylase (ACCase), malonyl Co A, fatty acid synthase (FAS) and carnitine palmitoyltransferase-1 (CPT-1), and the changes of hepatic tissue ACCase and CPT-1 m RNA levels. Results: The hepatic steatosis and vacuolar degeneration were observed in the model group. The contents of TG, FFA, ACCase, FAS, Malonyl Co A and ACCase m RNA in the model group were significantly higher than those in the normal group (P <0.01) , CPT-1 content and m RNA levels were significantly lower than the normal group (P <0.01). The above pathological changes in salidroside group were significantly reduced. The content of TG, FFA, ACCase, FAS, FAS and ACCase mRNA in liver tissues were significantly lower than those in model group (P <0.01) Significantly higher than the model group (P <0.01). Conclusion: Salidroside can inhibit liver fat synthesis, and promote fatty acid oxidation, which may be its prevention and treatment of non-alcoholic fatty liver disease is an important mechanism.