Intervention effect of salidroside on liver fat synthesis and oxidation of non-alcoholic fatty liver in rats induced by high-fat diet
- 医学院－已发表论文 
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 (Mallonyl CoA)、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ACCaseCPT-1; mRNA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; CoA含量和ACCase; mRNA水平较正常组均显著升高(P<0.01),CPT-1含量和mRNA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 CoA、FAS含量和ACCase mRNA水平显著低于模型组(P<0.01) ,; CPT-1含量和; mRNA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 explore the mechanism of salidroside on non-alcoholic; fatty liver disease based on liver fat synthesis and oxidation. Methods:; Non-alcoholic fatty liver disease model was induced by high-fat diet for; 14 weeks. From the ninth week, the rats were randomly divided into model; group, salidroside group and rosiglitazone group, and were given a; gavage for six weeks. The observing items including: pathological; changes of liver tissue (HE staining); changes of contents of; triglycerides (TG) and free fatty acid (FFA) in liver tissue; changes of; contents of acetyl-Coacarboxylase (ACCase), malonyl CoA, fatty acid; synthase(FAS) and carnitine palmitoyl transterase-l(CPT-l); changes of; mRNA levels of ACCase and CPT-1 in liver tissue. Results: Hepatocellular; steatosis and vacuolar degeneration were observed in the liver tissue of; the model group. The contents of TG, FFA, ACCase, Malonyl CoA, FAS and; mRNA level of ACCase in model group were significantly higher than those; of the normal group (P<0.01). The content and mRNA level of CPT-1 were; significantly lower than those of normal group (P<0.01). Hepatic; pathological changes in salidroside group were significantly reduced.; The contents of TG, FFA, ACCase, Malonyl CoA, FAS and mRNA level of; ACCase were significantly lower than those of model group (P<0.01). The; content and mRNA level of CPT-1 were significantly higher than those of; model group (P<0.01). Conclusion: Salidroside can inhibit liver fat; synthesis and promote the oxidation of fatty acid, which may be an; important mechanism of salidroside for prevention and treatment of; non-alcoholic fatty liver disease.