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作 者:张傲 李然[1] 刘立萍[1] ZHANG Ao;LI Ran;LIU Li-ping(Liaoning University of Traditional Chinese Medicine,Shenyang,Liaoning 110847,China)
出 处:《时珍国医国药》2024年第8期1882-1885,共4页Lishizhen Medicine and Materia Medica Research
基 金:中国博士后科学基金第九批特别资助项目(2016T90229);辽宁省科技厅自然科学基金计划重点项目(20170540618)。
摘 要:目的 观察苓桂术甘汤对FFA诱导的HepG2细胞脂质代谢的影响,探讨其作用机制是否与其干预FXR途径有关。方法 选用HepG2细胞,采用1mmol/L FFA诱导,实验分为正常组、模型组、苓桂术甘汤组、阿托伐他汀组。采用CCK-8法测定细胞活力,油红O染色法观察脂滴分布,生物试剂盒测定TG、TC含量,蛋白免疫印迹法检测FXR、SHP、CYP7A1、LXR、SREBP-1蛋白的表达量,免疫荧光法检测FXR的荧光表达强度。结果 与正常组相比,模型组脂滴分布增加,TG、TC含量升高(P<0.01),FXR、SHP蛋白表达水平降低,CYP7A1、LXR和SREBP-1蛋白表达水平升高,FXR荧光表达水平降低;与模型组比较,苓桂术甘汤组和阿托伐他汀组脂滴分布下降,TG、TC含量降低(P<0.01),FXR、SHP蛋白表达水平升高,CYP7A1、LXR和SREBP-1蛋白表达水平降低,FXR荧光表达水平升高。结论 苓桂术甘汤可显著抑制游离脂肪酸诱导的HepG2细胞脂肪沉积,其作用机制可能与干预FXR介导的脂质代谢通路有关。Objective To observe the effect of Linggui Zhugan decoction on the lipid metabolism of HepC2 cells by free fatty acid-induced,and to investigate whether the mechanism of intervention with FXR.Methods HepG2 cells were selected and induced by 1mmol/L FFA,and the experiments were divided into normal group and model group and Linggui Zhugan decoction group and atorvastatin group.Cell viability was determined by CCK-8;the distribution of lipid droplets was observed by oil red O staining;cellular TG and TC content by biological kit;cellular FXR,SHP,CYP7A1,LXR and SREBP-1 protein expression by Western blot;FXR by immunofluorescence.Results Compared with the normal group,in the model group,lipid droplet distribution in-creased,TG and TC content increased(P<O.O1),FXR and SHP protein expression levels were decreased,higher protein ex-pression levels of CYP7A1,LXR and SREBP-1,FXR fluorescence expression levels were decreased.Compared with the model group,lower lipid droplet distribution in the Linggui Zhugan decoction and atorvastatin groups,TG and TC content was decreased(P<0.O1),FXR and SHP protein expression levels were increased,the protein expression levels of CYP7A1,LXR and SREBP-1 were decreased,FXR fluorescence expression levels were increased.Conclusion Linggui Zhugan decoction significantly in-hibited on the lipid metabolism of HepG2 cells by free fatty acid-induced,the mechanism of action may be related to the inter-vention of FXR mediated lipid metabolism pathway.
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