【摘要】：目的探討NADPH氧化酶在高脂誘導的人臍靜脈血管內(nèi)皮細胞(human umbilical vein endothelial cells,HUVECs)氧化應激損傷中的作用。方法不同濃度(0.1、0.2、0.4、0.8 mmol·L~(-1))棕櫚酸(palmitic acid,PA)刺激HUVECs 0、12、24、48 h,CCK-8法檢測血管內(nèi)皮細胞增殖能力;免疫印跡法檢測血管內(nèi)皮細胞NADPH氧化酶亞基p22phox、p47phox、p67phox、gp91phox的表達水平;免疫熒光法檢測血管內(nèi)皮細胞細胞內(nèi)活性氧簇(reactive oxygen species,ROS)的表達水平。結果 0.4 mmol·L~(-1)PA刺激HUVECs 24、48 h組的細胞增殖率出現(xiàn)明顯降低。因此,實驗中我們采用0.4 mmol·L~(-1)PA刺激24 h作為模型組;0.4 mmol·L~(-1)PA刺激HUVECs24、48 h時,p22phox、p47phox、p67phox、gp91phox的表達均明顯升高(P0.05),24 h組與48 h組差異不明顯(P0.05);0.4mmol·L~(-1)PA刺激血管內(nèi)皮細胞24、48 h時,細胞內(nèi)ROS表達水平均明顯增高(P0.05),24 h組與48 h組差異不明顯(P0.05);與模型組(0.4 mmol·L~(-1)PA刺激24 h)相比,NADPH氧化酶抑制劑diphenyliodonium(DPI,10μmol·L~(-1))預處理可以使模型組血管內(nèi)皮細胞ROS表達水平明顯下調(diào)(P0.05)。結論 NADPH氧化酶活性對高脂所致血管內(nèi)皮細胞氧化應激損傷的防治有重要意義。
[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.
【作者單位】： 延邊大學附屬醫(yī)院心血管內(nèi)科;延邊大學附屬醫(yī)院中心實驗室;
【基金】：湖北省教育廳科學研究計劃項目(No B201696) 湖北科技學院糖尿病專項基金項目(No 2016-18XZ09)
【分類號】：R54

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