鸡骨草总黄酮碳苷对乙硫氨酸导致的小鼠脂肪肝的影响简

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／kgDL-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（Sterolregulatoryelementbind-ingprotein1，SREBP-1）、脂肪酸合成酶（Fattyacidsynthase，FAS）和乙酰辅酶A羧化酶（Aee-tyl-CoAcarboxylase1，ACCl）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（Peroxisomeproliferatoractivativedre-ceptora，PPARα）和肉碱棕榈酰转移酶1α（Carnitinepalmitoyltransferase1α，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。

Protective effect of total Flavonoid C-glycosides from Abrus mollis ex- tract on fatty liver induced by DL-Ethionine in mice

AIM： To study the effect of total flavonoid C-glycosides from Abrus mollis extract（AME） on lipid dysregulation induced by Ethi onine （DL-E）. METHODS： ICR mice were randomly assigned to four groups （n=8） ; Control, DL-E, AME and AME＋DL-E groups. Mice were gavaged with AME （200 mg/kg） for 7 days. At day 7, mice of DL-E and AME＋DL-E group were gavaged with DL-E （250 mg/kg）, other two groups were treated with vehicle con- trol （0.2% CMC-Na）. Serum and liver tissues were collected 22 h after administration of DL- E. The contents of hepatic lipids, serum lipids and ALT, AST levels were measured. The ex- pressions of key genes involved in lipid metabo- lism were also observed by real-time PCR. RE- SULTS：The results indicated that AME provided significant protection against fatty liver by inhib- iting the elevation of serum lipids, serum trans- aminase, reducing hepatic TG and TC accumula-tion, ameliorating the severity of pathological changes. Furthermore, AME significantly de- creased DL-E-induced SREBP-1, FAS and ACC1 high expressions, which resulting in the lipid homeostasis. The down-regulation of CPT-1α and PPARα that reflect fatty acid metabolism in- duced by DL-E were reversed by AME treat- ment. CONCLUSION： The results indicated AME has hepatoprotective effect on Ethionine- induced fatty liver in mice and the effect was mostly due to the regulation on lipid synthesis and fatty acid metabolism.