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作 者:张鹏 张年荣 谢紫洁 欧阳昌汉[1] 余开湖[1,2] ZHANG Peng;ZHANG Nian-rong;YU Kai-hu(Hubei University of Science and Technology,Xianning Hubei 437100,China)
机构地区:[1]湖北科技学院,湖北咸宁437100 [2]湖北科技学院附属第一医院放射介入科,湖北咸宁437100
出 处:《湖北科技学院学报(医学版)》2020年第3期208-213,F0002,共7页Journal of Hubei University of Science and Technology(Medical Sciences)
基 金:国家自然科学基金面上项目(81571644);湖北科技学院药学重点学科专项科研项目(2018-19XYZ08)。
摘 要:目的探讨自噬受体蛋白(FUNDC1)过表达对高脂诱导的EA.hy926人血管内皮细胞的保护作用。方法通过腺病毒过表达EA.hy926人血管内皮细胞中FUNDC1,加入棕榈酸建立高脂细胞模型;实验分为对照组、高脂组、高脂+空载组、高脂+FUNDC1组;分别检测各组细胞增殖活性、活性氧含量、细胞线粒体膜电位、ATP含量及自噬相关蛋白表达。结果与高脂组比较,高脂+FUNDC1组存活率显著上升(P<0.01)、活性氧含量显著下降(P<0.01)、膜电位去极化比例显著下降(P<0.01)、ATP含量显著上升(P<0.05);对于LC3、P62的表达水平,高脂组、高脂+空载组与对照组比较显著上升(P<0.05),高脂+FUNDC1组与高脂组比较显著下降(P<0.05)。结论FUNDC1通过介导自噬,对高脂诱导的人血管内皮细胞EA.hy926有保护作用。Objective To investigate the protective effect of FUNDC1 overexpression against hyperlipidemia induced human vascular endothelial cells EA.hy926 injury.Methods Adenovirus was used to overexpress FUNDC1 in EA.hy926 human vascular endothelial cells,and then palmitic acid was added to establish a cell model of lipotoxicity.The experiment was divided into 4 groups:control group,lipotoxicity group,lipotoxicity+empty adenovirus group,lipotoxicity+FUNDC1 adenovirus group.The cell proliferation activity,reactive oxygen content,cell mitochondrial membrane potential,ATP content and autophagy-related protein expression were detected in each group.Results Compared with the lipotoxicity group,the survival rate of the lipotoxicity+FUNDC1 group increased significantly(P<0.01),the ROS decreased significantly(P<0.01),the membrane potential depolarization ratio decreased significantly(P<0.01),and the ATP content increased significantly(P<0.05).For the protein expression of LC3 and P62,the lipotoxicity group,lipotoxicity+empty adenovirus group increased significantly compared with the control group(P<0.05),and the lipotoxicity+FUNDC1 group decreased significantly compared with the lipotoxicity group(P<0.05).Conclusion FUNDC1 has a protective effect against hyperlipidemia induced human vascular endothelial cells EA.hy926 injury via mediating autophagy.
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