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目的 :探讨人巨细胞病毒 (HCMV)在动脉粥样硬化 (AS)发生和发展中的作用及可能的机制。方法和结果 :采用组织培养技术和流式细胞计数仪观察HCMV对离体培养的HUVEC凋亡的影响。实验发现无血清培养和TNF诱导的细胞凋亡率较正常对照组升高 ,而CMV感染组凋亡率明显降低。用流式细胞仪检测发现 ,在DNA直方图上 ,在G1峰左侧可呈现亚二倍体核峰型 (亚G1峰 ,即凋亡峰 )。而正常的细胞经流式细胞仪检测 ,没有亚二倍体细胞群的峰型 ;CMV可以抑制HUVEC的一氧化氮 (NO)的合成 ,并且呈浓度依赖性。结论 :HCMV感染HUVEC后能够抑制HUVEC的细胞凋亡 ,可能的介导因素为被HCMV感染的HUVEC其NO合成减少。
Objective: To investigate the role and possible mechanism of human cytomegalovirus (HCMV) in the development and progression of atherosclerosis (AS). Methods and Results: The effects of HCMV on the apoptosis of HUVECs cultured in vitro were observed using tissue culture techniques and flow cytometry. The results showed that serum-free culture and TNF-induced apoptosis rate increased compared with the normal control group, while the apoptosis rate of CMV infection group was significantly reduced. Flow cytometry showed that in the DNA histogram, the sub-diploid nuclear peak (sub-G1 peak, the apoptotic peak) appeared on the left of the G1 peak. The normal cells were detected by flow cytometry, there is no subduploid cell population peak; CMV can inhibit HUVEC nitric oxide (NO) synthesis, and in a concentration-dependent manner. CONCLUSION: HUVEC infected with HCMV can inhibit the apoptosis of HUVEC. The possible mediating factor is the decrease of NO synthesis in HUVEC infected with HCMV.