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HCV刺激人脐静脉内皮细胞发生动脉粥样硬化的机制
Mechanism of HCV stimulation of human umbilical vein endothelial cells in the pathogenesis of atherosclerosis
文章发布日期:2019年05月13日  来源:  作者:朱紫衣,刘媛,王文博,等  点击次数:186次  下载次数:36次

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【摘要】:目的以HCV体外刺激人脐静脉内皮细胞(HUVECs)为模型,探讨HCV感染致动脉粥样硬化发生的机制。方法采用1.0 MOI HCV病毒颗粒刺激HUVECs,CCK8检测细胞增殖;流式细胞仪检测细胞凋亡及周期;划痕实验及单核内皮黏附实验评估HCV对HUVECs迁移及黏附能力的影响;荧光定量PCR及Western blot检测HCV刺激HUVECs炎症因子及内皮损伤因子的表达。2组间比较采用两独立样本t检验,多组间比较采用方差分析,进一步两两比较采用LSD-t检验。结果与对照组比较,HCV对HUVECs的生长增殖、细胞凋亡及周期无明显影响(P值均>0.05)。HCV刺激抑制了HUVECs的迁移能力,而增强其黏附能力。与对照组比较,HCV刺激促进内皮细胞炎症因子IL-6、IL-1β以及趋化因子CXCL10、单核细胞趋化蛋白-1 mRNA水平升高(t值分别为-10.155、-12.048、-5.025、-20.116,P值均<0.05)及蛋白表达增加(F值分别为2541.739、4806.490、477.608、501380,P值均<0.001)。HCV刺激导致HUVECs内皮损伤因子内皮素-1、血管内皮生长因子以及黏附分子—细胞间黏附分子-1、血管细胞黏附因子-1表达上调(t值分别为-4.530、-4.497、-7.692、-7.449,P值均<0.05)。结论HCV可以引起内皮细胞炎症改变和功能障碍,影响动脉粥样硬化的发生。
【Abstract】:ObjectiveTo investigate the mechanism of HCV infection in the pathogenesis of atherosclerosis with a model of human umbilical vein endothelial cells (HUVECs) stimulated by HCV in vitro. MethodsHUVECs were stimulated with 1.0 MOI HCVcc for 48 hours. CCK8 assay was used to measure cell proliferation; flow cytometry was used to measure cell apoptosis and cell cycle; wound healing assay and monocyte-endothelial adhesion assay were used to evaluate the influence of HCV on the migration and adhesion of HUVECs; quantitative real-time PCR and Western blot were used to measure the expression of inflammatory factors and endothelial injury factors in HUVECs stimulated by HCV. The two-independent-samples t test was used for comparison between two groups; an analysis of variance was used for comparison between multiple groups, and the LSD-t test was used for further comparison between two groups. ResultsCompared with the control group, the HCV group had no significant changes in the growth, apoptosis, and cell cycle of HUVECs (all P>0.05). HCV stimulation inhibited the migration of HUVECs and enhanced their adhesion ability. Compared with the control group, the HCV group had significant increases in the mRNA and protein expression of the inflammatory factors interleukin-6 and interleukin-1β and the chemokines CXCL10 and monocyte chemotactic protein 1 (mRNA expression: t=-10.155, -12.048, -5.025, and -20.116, all P<0.05; protein expression: F=2541.739, 4806.490, 477.608, and 501.38, all P<0.001). HCV stimulation significantly upregulated the expression of the endothelial injury factors endothelin-1 and vascular endothelial growth factor and the adhesion molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in HUVECs (t=-4.530, -4.497, -7.692, and -7.449, all P<0.05). ConclusionHCV can cause inflammatory changes and dysfunction in endothelial cells and thus affect the development of atherosclerosis.
【关键字】:肝炎病毒属; 人脐静脉内皮细胞; 动脉粥样硬化
【Key words】:hepacivirus; human umbilical vein endothelial cells; atherosclerosis
【引证本文】:ZHU ZY, LIU Y, WANG WB, et al. Mechanism of HCV stimulation of human umbilical vein endothelial cells in the pathogenesis of atherosclerosis[J]. J Clin Hepatol, 2019, 35(6): 1313-1317. (in Chinese)
朱紫衣, 刘媛, 王文博, 等. HCV刺激人脐静脉内皮细胞发生动脉粥样硬化的机制[J]. 临床肝胆病杂志, 2019, 35(6): 1313-1317.

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