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目的:探讨人巨细胞病毒(HCMV)对人脐静脉内皮细胞(HUVEC304)细胞周期和凋亡的影响和机制及银杏黄酮苷对其感染HUVEC304的作用。方法:实验分为4组,分别为正常对照组、银杏黄酮苷组、HCMV感染组、HCMV感染加银杏黄酮苷组。采用流式细胞技术对HCMV感染的体外培养的HUVEC304及银杏黄酮苷对其作用后进行观察和分析。结果:HCMV感染HUVEC304后24h,正常对照组G0/G1期的细胞为74.4%,加入HCMV后为59.3%,较正常对照组降低20.3%(P<0·05)。正常对照组凋亡细胞为8.3%,当加入HCMV后为5.8%,较正常对照组降低30.1%(P<0·01)。银杏黄酮苷可以降低HCMV增加进入S和G2/M期的细胞,HCMV感染的细胞处在G0/G1期的为59.3%,用10-2mol/L银杏黄酮苷后被感染细胞处在G0/G1期的增加为67.5%,较感染组增加13.8%(P<0·05)。银杏黄酮苷可以增加HCMV感染的HUVEC304凋亡水平。HCMV感染后凋亡细胞为5.8%,加入10-2mol/L银杏黄酮苷后凋亡细胞为6.2%,较HCMV组升高6.9%(P<0·05)。结论:HCMV感染HUVEC304后,可以降低HUVEC304停留在G1期的细胞,使进入S和G2/M期的细胞明显增加,表明HCMV感染早期可通过增加G0/G1期细胞进入S和G2/M期,导致细胞最终表现为增殖。应用银杏黄酮苷可以促进细胞从G1期向S和G2/M期的转化和细胞的凋亡。HCMV感染HU-VEC304引起的炎性反应可能影响内皮细胞的功能,导致血栓形成、脂质代谢紊乱,最终参与动脉粥样硬化的形成。而银杏黄酮苷可促进HCMV感染HUVEC304的凋亡,抑制被感染细胞的过度增生,因而可能对防治动脉粥样硬化有一定的作用。
Objective: To investigate the effect and mechanism of human cytomegalovirus (HCMV) on the cell cycle and apoptosis of human umbilical vein endothelial cells (HUVEC304) and the effects of flavonoid glycosides of Ginkgo biloba on the infection of HUVEC304. Methods: The experiment was divided into 4 groups: normal control group, ginkgo flavone glycoside group, HCMV infection group, HCMV infection plus ginkgo flavonoid glycoside group. Flow cytometry was used to observe and analyze the effects of HCMV-infected HUVEC304 and Ginkgo biloba flavonoids in vitro. Results: 24 h after HCMV infection of HUVEC304, 74.4% of cells in the G0/G1 phase of the normal control group, 59.3% after adding HCMV, 20.3% lower than the normal control group (P <0. 05). The apoptotic cells in the normal control group were 8.3%, 5.8% after the addition of HCMV, a decrease of 30.1% compared with the normal control group (P<0.01). Ginkgo flavonoid glycosides decreased the number of HCMV-infected cells entering the S and G2/M phases. HCMV-infected cells were in G0/G1 phase at 59.3%, and infected cells at G0/G1 with 10-2 mol/L ginkgo flavonoid glycosides. The increase of the period was 67.5%, which was 13.8% higher than that of the infection group (P<0.05). Ginkgo flavonoid glycosides can increase the apoptosis of HCMV-infected HUVEC304. Apoptotic cells were 5.8% after HCMV infection, and apoptotic cells were 6.2% after adding 10-2 mol/L ginkgo flavonoid glycoside, which was 6.9% higher than that of HCMV group (P<0.05). Conclusion: After HCMV infection of HUVEC304, HUVEC304 can reduce the number of cells staying in G1 phase and increase the number of cells entering S and G2/M phases. This indicates that HCMV infection can increase the number of G0/G1 phase cells into S and G2/M phase. The resulting cells eventually appear to proliferate. Ginkgo flavonoid glycosides can promote cell transformation from G1 phase to S and G2/M phase and cell apoptosis. The inflammatory reaction induced by HCMV infection of HU-VEC304 may affect the function of endothelial cells, leading to thrombosis, disorder of lipid metabolism, and finally participate in the formation of atherosclerosis. Ginkgo flavonoid glycosides can promote the apoptosis of HUVEC304 infected by HCMV and inhibit the hyperplasia of infected cells, which may play a role in the prevention and treatment of atherosclerosis.