环氧化酶-2与单核-内皮细胞黏附性的相关研究被引量：1

The research of the relationship between Cyclooxygenase-2 and monocyte-endothelial cells adhesion

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摘要目的探讨环氧化酶-2(Cyclooxygenase-2,COX-2)表达水平同单核-内皮细胞黏附性的关系及其相关机制。方法采用细胞计数法检测单核-内皮细胞的黏附性;实时荧光定量PCR检测内皮细胞COX-2mRNA表达量;Western blot检测内皮细胞COX-2蛋白表达量;ELISA检测内皮细胞前列腺素E2(Prostaglandin E2,PGE2)水平。结果内皮细胞COX-2mRNA及蛋白表达量在炎症因子TNF-α、IL-1β刺激后显著上调,并随时间变化(P<0.05);内皮细胞COX-2蛋白表达量增加与PGE2水平及单核-内皮细胞的黏附性成正相关;使用COX-2特异性抑制剂NS398预孵育后,内皮细胞PGE2表达水平降低(P<0.05),单核-内皮细胞的黏附性受到显著抑制(P<0.01)。结论内皮细胞COX-2mRNA及蛋白表达量在炎症因子TNF-α、IL-1β刺激后明显上调,其表达增加后可能通过催化花生四烯酸代谢成PGE2,使单核-内皮细胞的黏附性增强,从而影响动脉粥样硬化性疾病的进程。 Objective To investigate the relationship between Cyclooxygenase-2 levels and monocyte-endothelial cells adhesion. Methods Monocyte-endotheliat cells adhesion was assessed by counting cells number. The expression of COX-2 mRNA and protein were measured by real-time PCR and Western blot assay. The expression of Prostaglandin E2 （PGE2） was performed by ELISA. Results Inflammatory cytokines TNF-α、IL-1β could significantly induce the ex- pression of COX-2 mRNA and protein in varying degrees（P〈0.05） ; High COX-2 levels could result in high PGE2 level and induce monocyte-endothelial cells adhesion signifieantly;COX-2 specific inhibitor NS398 significantly inhibited the inflammatory cytokines induced PGE2 expression （P〈0.05）,then affecting monoeyte-endothelial cells adhesion （P〈 0.01）. Conclusion Inflammatory cytokines TNF-α、IL-1β could induce the expression of COX-2, which could induce the expression of PGE2 ,monocyte-endothelial cells adhesion and then could affect the progress of the atheroselerotic dis- ease.

作者王红艳徐春亮蔡凡曹久妹陈晓南吴方

机构地区上海交通大学医学院附属瑞金医院老年病科上海交通大学医学院中国科学院上海生命科学研究院健康科学研究中心

出处《中国实验诊断学》 2013年第10期1743-1746,共4页 Chinese Journal of Laboratory Diagnosis

基金上海市科委基金(124119a6800) 上海市教委基金(11YZ57)

关键词动脉粥样硬化环氧化酶-2 人主动脉内皮细胞单核-内皮细胞黏附前列腺素E2 Atherosclerosis Cyclooxygenase-2 Human aortic endothelial cell Monocyte-endothelial ceils adhesion PGE2

分类号 R543.5 [医药卫生—心血管疾病]

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