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目的:研究鸡骨草总黄酮碳苷(AME)对乙硫氨酸(DL-E)所致小鼠脂肪肝的影响,并探讨其作用机制。方法:ICR小鼠随机分为4组:对照组,DL-E造模组,AME组和AME+DL-E组,每组8只。用AME连续灌胃给予AME组和AME+DL-E组小鼠7d,另外两组给予溶剂对照(三蒸水),第7天灌胃给予DL-E组和AME+DL-E组250mg/kg DL-E造模,其他两组给予溶剂对照(0.2%CMC-Na)。造模1h后再次灌胃给予所有小鼠AME或溶剂对照(三蒸水),造模22h后收集血样和肝组织,采用生化法测定血清脂质和转氨酶水平,肝脏TG以及TC含量。采用实时定量PCR的方法测定肝脏中相关脂代谢基因水平。结果:AME可以显著减少小鼠肝脏脂肪空泡的数量和脂变的面积,降低TG和TC含量以及血清转氨酶水平。在脂质相关代谢基因的调控上,AME可以下调DL-E导致的固醇调节元件结合蛋白-1(Sterol regulatory element binding protein 1,SREBP-1)、脂肪酸合成酶(Fatty acid synthase,FAS)和乙酰辅酶A羧化酶(Acetyl-CoA carboxylase 1,ACC1)的高表达,并且AME可以逆转DL-E对过氧化物酶体增殖物活化受体α(Peroxisome proliferator activatived receptorα,PPARα)和肉碱棕榈酰转移酶1α(Carnitine palmitoyltransferase 1α,CPT-1α)的抑制作用。结论:AME对DL-E引起的小鼠肝脏脂肪蓄积具有保护作用,并且这种作用主要是通过减少脂质合成,促进脂质氧化代谢来实现的。
Objective: To study the effect of total flavonoids of Abrus cantoniensis (AME) on fatty liver in mice induced by ethionine (DL-E) and to explore its mechanism. Methods: ICR mice were randomly divided into 4 groups: control group, DL-E model group, AME group and AME + DL-E group, 8 rats in each group. The mice in AME group and AME + DL-E group were administered intragastrically with AME for 7 days. The other two groups were given solvent control (triple distilled water). The mice in DLE group and AME + DL-E group were given 250 mg / kg DL-E, and the other two groups were given solvent control (0.2% CMC-Na). All rats were given intragastric administration of AME or solvent control (triple distilled water) 1 h after model establishment. Blood samples and liver tissues were collected 22 h after modeling. Serum lipid and aminotransferase levels, liver TG and TC contents were determined by biochemical methods. Real-time quantitative PCR was used to determine the level of related lipid metabolism genes in the liver. Results: AME could significantly reduce the number of hepatic steatosis and the areas of lipid peroxidation in mice, lower the content of TG and TC, and the level of serum aminotransferase. AME can down regulate the expression of sterol regulatory element binding protein 1 (SREBP-1), fatty acid synthase (FAS) and Acetyl-CoA carboxylase 1 (ACC1) and AME can reverse the effect of DL-E on Peroxisome proliferator activated receptor α (PPARα) and carnitine Inhibition of Carnitine palmitoyltransferase 1α (CPT-1α). Conclusion: AME has a protective effect on the liver fat accumulation induced by DL-E in mice, and this effect is mainly achieved by reducing lipid synthesis and promoting lipid oxidation metabolism.