HCV刺激人脐静脉内皮细胞发生动脉粥样硬化的机制

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...

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Published inLinchuang gandanbing zazhi Vol. 35; no. 6; pp. 1313 - 1317
Main Authors 朱紫衣, 刘媛, 王文博, 江忠勇, 常凯, 叶雨笙, 熊杰
Format Journal Article
LanguageChinese
Published Changchun Journal of Clinical Hepatology 01.06.2019
西部战区总医院检验科,成都,610083%西部战区疾病预防控制中心,成都,610021
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ISSN1001-5256
2097-3497
DOI10.3969/j.issn.1001-5256.2019.06.026

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Abstract 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) 。...
AbstractList R512.63%R543.4; 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.
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) 。...
Author 王文博
江忠勇
熊杰
刘媛
朱紫衣
叶雨笙
常凯
AuthorAffiliation 西部战区总医院检验科,成都,610083%西部战区疾病预防控制中心,成都,610021
AuthorAffiliation_xml – name: 西部战区总医院检验科,成都,610083%西部战区疾病预防控制中心,成都,610021
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  fullname: 熊杰
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Keywords 肝炎病毒属
人脐静脉内皮细胞
动脉粥样硬化
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PublicationTitle Linchuang gandanbing zazhi
PublicationTitle_FL Journal of Clinical Hepatology
PublicationYear 2019
Publisher Journal of Clinical Hepatology
西部战区总医院检验科,成都,610083%西部战区疾病预防控制中心,成都,610021
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Snippet 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...
R512.63%R543.4; 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...
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StartPage 1313
SubjectTerms Apoptosis
Atherosclerosis
Cell cycle
Cytokines
Pathogenesis
Protein expression
Proteins
Title HCV刺激人脐静脉内皮细胞发生动脉粥样硬化的机制
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