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作 者:王喆 王宇琪 张彩云 袁凤霞 徐天缘 朱穆朗玛 崔元赫 王湘琪 朴光春[1] 元海丹[1] WANG Zhe;WANG Yuqi;ZHANG Caiyun;YUAN Fengxia;XU Tianyuan;ZHU Mulangma;CUI Yuanhe;WANG Xiangqi;PIAO Guangchun;YUAN Haidan(Yanbian University College of Pharmacy,Yanji 133002,Jilin,China)
出 处:《延边大学医学学报》2023年第2期103-106,共4页Journal of Medical Science Yanbian University
基 金:吉林省大学生创新创业训练计划项目(编号:S202210184037);国家自然科学基金项目(81660614;82060674)。
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.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.
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