HCV刺激人脐静脉内皮细胞发生动脉粥样硬化的机制

朱紫衣; 刘媛; 王文博; 江忠勇; 常凯; 叶雨笙; 熊杰

doi:10.3969/j.issn.1001-5256.2019.06.026

HCV刺激人脐静脉内皮细胞发生动脉粥样硬化的机制

DOI: 10.3969/j.issn.1001-5256.2019.06.026

1. 西部战区总医院检验科
2. 西部战区疾病预防控制中心

基金项目:

四川省科技厅资助项目(2013JY0173)；中国博士后科学基金(2017T100820,2018T111157)；

详细信息

中图分类号: R512.62
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出版历程
- 收稿日期: 2019-01-24
- 出版日期: 2019-06-20

Mechanism of HCV stimulation of human umbilical vein endothelial cells in the pathogenesis of atherosclerosis

Department of Clinical Laboratory, The General Hospital of Western Theater Command

Research funding:

摘要

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）。...
- 肝炎病毒属 /
- 人脐静脉内皮细胞 /
- 动脉粥样硬化
Abstract:
Objective To 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. Methods HUVECs 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. Results Compared 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) . Conclusion HCV can cause inflammatory changes and dysfunction in endothelial cells and thus affect the development of atherosclerosis.
- hepacivirus /
- human umbilical vein endothelial cells /
- atherosclerosis

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