血管内皮生长因子拮抗缺氧诱导的血管内皮细胞凋亡及其机制研究  

Effect and mechanical study of vascular endothelial growth factor on inhibition apoptosis of vascular endothelial cell induced by hypoxia

作　　者：廖德荣[1] 刘启功[1] 程燕子[1] 曾艳[1] 张兹伟[2] 

机构地区：[1]华中科技大学同济医学院附属同济医院心内科,湖北武汉430030 [2]湖北城市建设职业技术学院,湖北武汉430074

出　　处：《中国现代医学杂志》2007年第22期2732-2735,共4页China Journal of Modern Medicine

基　　金：湖北省自然科学基金项目(No:2003ABA135)

摘　　要：目的研究血管内皮生长因子(VEGF)和缺氧对血管内皮细胞凋亡及凋亡相关基因Bcl-2与Apo-1/FasmRNA表达的影响,探讨VEGF用于预防经皮冠状动脉介入治疗术(PCI)后再狭窄的机制。方法将体外培养的人脐静脉内皮细胞(hUVEC)分成对照组、缺氧处理组、缺氧+VEGF处理组,12h后采用原位末端标记法、流式细胞术观察各组细胞的凋亡发生情况,通过RT-PCR法观察各组细胞中凋亡相关基因Bcl-2与Apo-1/FasmRNA表达的变化。结果与对照组和缺氧+VEGF处理组比较,缺氧处理组凋亡细胞及FasmRNA表达明显增加,Bcl-2mRNA表达明显下降,而VEGF能拮抗上述作用。结论VEGF能拮抗缺氧诱导的内皮细胞凋亡,其抗凋亡的机制可能与上调Bcl-2mRNA表达与下调Apo-1/FasmRNA表达有关。从而为VEGF预防再狭窄进一步提供了理论依据。[Objective] To study the mechanism of vascular endothelial growth factor （VEGF） on prevention of restenosis after percutaneous coronary intervention （PCI） by observing the effect of VEGF and hypoxia on the apoptosis of vascular endothelial cell. [Method] Human umbilical vein endothelial cells （hUVEC） were divided into control group, hypoxia-treated group and hypoxia ＋VEGF-treated group, and apoptosis of hUVEC was determined by FCM and TUNEL, and the expression of Bcl-2 mRNA and Fas mRNA was examined by RT-PCR. [Result] Compared with control group and hypoxia ＋VEGF-treated group, in hypoxia-treated group, the apoptosis cells and the expression of Fas mRNA significantly increased, the expression of Bcl-2 mRNA markedly decreased, but VEGF could inhibit the effect of hypoxia on hUVEC. [Conclusion] VEGF could inhibit the apoptosis of hUVEC induced by hypoxia via downregulation of Fas mRNA expression and upregulation of Bcl-2 mRNA expression, which offered further theoretical evidence for VEGF on prevention of restenosis after PCI.

关 键 词：血管内皮生长因子 细胞凋亡 缺氧 

分 类 号：R331[医药卫生—人体生理学]