NADPH氧化酶在高脂诱导的人脐静脉血管内皮细胞氧化应激损伤中的作用
发布时间：2019-01-28 07:09
【摘要】：目的探讨NADPH氧化酶在高脂诱导的人脐静脉血管内皮细胞(human umbilical vein endothelial cells,HUVECs)氧化应激损伤中的作用。方法不同浓度(0.1、0.2、0.4、0.8 mmol·L~(-1))棕榈酸(palmitic acid,PA)刺激HUVECs 0、12、24、48 h,CCK-8法检测血管内皮细胞增殖能力;免疫印迹法检测血管内皮细胞NADPH氧化酶亚基p22phox、p47phox、p67phox、gp91phox的表达水平;免疫荧光法检测血管内皮细胞细胞内活性氧簇(reactive oxygen species,ROS)的表达水平。结果 0.4 mmol·L~(-1)PA刺激HUVECs 24、48 h组的细胞增殖率出现明显降低。因此,实验中我们采用0.4 mmol·L~(-1)PA刺激24 h作为模型组;0.4 mmol·L~(-1)PA刺激HUVECs24、48 h时,p22phox、p47phox、p67phox、gp91phox的表达均明显升高(P0.05),24 h组与48 h组差异不明显(P0.05);0.4mmol·L~(-1)PA刺激血管内皮细胞24、48 h时,细胞内ROS表达水平均明显增高(P0.05),24 h组与48 h组差异不明显(P0.05);与模型组(0.4 mmol·L~(-1)PA刺激24 h)相比,NADPH氧化酶抑制剂diphenyliodonium(DPI,10μmol·L~(-1))预处理可以使模型组血管内皮细胞ROS表达水平明显下调(P0.05)。结论 NADPH氧化酶活性对高脂所致血管内皮细胞氧化应激损伤的防治有重要意义。
[Abstract]:Objective to investigate the role of NADPH oxidase in hyperlipidemic induced oxidative stress injury of human umbilical vein endothelial cells (human umbilical vein endothelial cells,HUVECs). Methods the proliferation ability of vascular endothelial cells was measured by CCK-8 method with different concentrations (0.1g / 0.42) and 0.8 mmol / L ~ (-1) palmitic acid (palmitic acid,PA) stimulated by HUVECs 012U 2448 h. The expression level of NADPH oxidase subunit p22phoxfen p47phoxfen p67phoxtgp91phox and reactive oxygen species (reactive oxygen species,ROS) in vascular endothelial cells were detected by immunoblotting and immunofluorescence respectively. Results the proliferation rate of 0.4 mmol L ~ (-1) PA was significantly decreased in the HUVECs 24 ~ (-1) 48 h group. Therefore, we used 0.4 mmol L ~ (-1) PA for 24 h as model group. When HUVECs24,48 was stimulated with 0.4 mmol L ~ (-1) PA, the expression of p22phoxtasone p47phoxtio p67phoxangp91phox was significantly increased (P0.05), but there was no significant difference between 24 h group and 48 h group (P0.05). When 0.4mmol L ~ (-1) PA stimulated vascular endothelial cells for 24 h, the expression of ROS increased significantly (P0.05), but there was no significant difference between 24 h group and 48 h group (P0.05). Compared with model group (0.4 mmol L ~ (-1) PA for 24 h), pretreatment with diphenyliodonium (DPI,10 渭 mol L ~ (-1) could significantly down-regulate the expression of ROS in vascular endothelial cells of model group (P0.05). Conclusion the activity of NADPH oxidase plays an important role in the prevention and treatment of vascular endothelial cell oxidative stress injury induced by hyperlipidemia.
【作者单位】： 延边大学附属医院心血管内科;延边大学附属医院中心实验室;
【基金】：湖北省教育厅科学研究计划项目(No B201696) 湖北科技学院糖尿病专项基金项目(No 2016-18XZ09)
【分类号】：R54
[Abstract]:Objective to investigate the role of NADPH oxidase in hyperlipidemic induced oxidative stress injury of human umbilical vein endothelial cells (human umbilical vein endothelial cells,HUVECs). Methods the proliferation ability of vascular endothelial cells was measured by CCK-8 method with different concentrations (0.1g / 0.42) and 0.8 mmol / L ~ (-1) palmitic acid (palmitic acid,PA) stimulated by HUVECs 012U 2448 h. The expression level of NADPH oxidase subunit p22phoxfen p47phoxfen p67phoxtgp91phox and reactive oxygen species (reactive oxygen species,ROS) in vascular endothelial cells were detected by immunoblotting and immunofluorescence respectively. Results the proliferation rate of 0.4 mmol L ~ (-1) PA was significantly decreased in the HUVECs 24 ~ (-1) 48 h group. Therefore, we used 0.4 mmol L ~ (-1) PA for 24 h as model group. When HUVECs24,48 was stimulated with 0.4 mmol L ~ (-1) PA, the expression of p22phoxtasone p47phoxtio p67phoxangp91phox was significantly increased (P0.05), but there was no significant difference between 24 h group and 48 h group (P0.05). When 0.4mmol L ~ (-1) PA stimulated vascular endothelial cells for 24 h, the expression of ROS increased significantly (P0.05), but there was no significant difference between 24 h group and 48 h group (P0.05). Compared with model group (0.4 mmol L ~ (-1) PA for 24 h), pretreatment with diphenyliodonium (DPI,10 渭 mol L ~ (-1) could significantly down-regulate the expression of ROS in vascular endothelial cells of model group (P0.05). Conclusion the activity of NADPH oxidase plays an important role in the prevention and treatment of vascular endothelial cell oxidative stress injury induced by hyperlipidemia.
【作者单位】： 延边大学附属医院心血管内科;延边大学附属医院中心实验室;
【基金】：湖北省教育厅科学研究计划项目(No B201696) 湖北科技学院糖尿病专项基金项目(No 2016-18XZ09)
【分类号】：R54
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