【摘要】 [目的]探讨科罗索酸（CA）对高脂饲料（HFD）诱导小鼠非酒精性脂肪肝的保护作用及其机制.[方法]选择5周龄C57BL/6j雄性小鼠随机分为5个组，即正常（CON）组、模型（HFD）组、CA低剂量（10 mg/kg CA,CAL）组、CA高剂量（20 mg/kg CA,CAH）组及阳性对照（300 mg/kg二甲双胍，MET）组.CON组给予10 kcal%正常饲料喂养，其余4个组均给予60 kcal%HFD喂养，共喂养13周，最后4周分别灌胃给予各组小鼠相应剂量的药物，每日1次.[结果]与HFD组比较，CAH组小鼠三酰甘油和总胆固醇水平均显著降低（P<0.001），肝脏组织脂滴蓄积明显减少（P<0.001）. CA呈剂量依赖性地激活小鼠肝脏组织中AMPK和ACC蛋白质的表达（P<0.001），抑制SREBP1c、FAS及SCD1等基因表达（P<0.001），并升高PPARα和CD36基因表达（P<0.001）.[结论]C A可能通过激活AMPK信号通路来调控肝脏脂质积蓄.更多还原

【Abstract】 OBJECTIVE To investigate the protective effect of corosolic acid(CA) on mice nonalchoholic fatty liver disease induced by high fat diet(HFD)and its mechanism. METHODS C57BL/6j male mice aged 5 weeks were randomly divided into 5 groups, control group(CON),model group(HFD), CA low dose group(10 mg/kg CA, CAL),CA high dose group(20 mg/kg CA, CAH) and positive control group(300 mg/kg metformin, MET). The CON group was fed with 10 kcal% normal diet, and the other 4 groups were fed with 60 kcal% HFD for 13 weeks. In the last 4 weeks, the mice in each group were given the corresponding dose of medication by gavage once a day. RESULTS Compared with the HFD group, the levels of triglyceride and total cholesterol in CAH group were significantly reduced(P<0.001), and the accumulation of lipid droplets in liver tissue was significantly reduced(P<0.001). CA activated the expressions of AMPK and ACC protein in mice liver in a dose-dependent manner(P<0.001), inhibited the expressions of SREBP1c, FAS, SCD1 and other genes(P<0.001), and increased the expressions of PPARα and CD36 genes(P<0.001). CONCLUSION CA might regulate lipid accumulation in the liver by activating AMPK signaling pathway.更多还原