中文摘要：

目的研究二苯乙烯苷（TSG）对过氧化氢（H2O2）诱导人脐静脉内皮细胞凋亡的作用,以及对抗凋亡基因Bcl-2表达的影响。方法体外培养人脐静脉内皮细胞,筛选造模内皮细胞凋亡的H2O2浓度,以不同浓度二苯乙烯苷作用24 h。采用MTT法检测细胞生长活力,Hoechst33258染色观察细胞形态,流式细胞仪检测细胞凋亡率,Western-blot检测Bcl-2蛋白的含量。结果过氧化氢能引起内皮细胞损伤,抑制细胞增殖,并且随着浓度增加,细胞生存率逐渐降低。其中300μmol/L H2O2作用后细胞增殖明显受到抑制,Hoechst33258染色可见大量凋亡细胞,流式细胞仪检测出明显的凋亡峰,Bcl-2蛋白的表达量显著减少;加入二苯乙烯苷作用后,随着TSG浓度增加,细胞生存率增加,凋亡率逐渐降低;与H2O2造模组比较,10μmol/L的二苯乙烯苷预处理能够显著提高细胞生存率,抑制细胞的凋亡,并且使Bcl-2表达增加（P〈0.05）。结论二苯乙烯苷能抑制过氧化氢诱导的内皮细胞凋亡,该作用与上调Bcl-2表达有关。

英文摘要：

Objective To investigate the effect and mechanism of tetrahydroxystilbene-2-O-β-D-glucoside（TSG） on the apoptosis of human umbilical vein endothelial cells（hUVECs） induced by hydrogen peroxide（H2O2）.Methods hUVECs treated with H2O2（100,200,300,400,500 μmol/L）and TSG（0.1,1,10,100 μmol/L）for 24 hours,the optimal concentration of hydrogen peroxide（H2O2） and TSG were selected by MTT,Hoechst33258 staining and Flow Cytometry.The expression of Bcl-2 was detected by Western-blot.Results H2O2 could induce endothelial cell injure and inhibition of cell proliferation.The cell proliferation rate was decreased and the apoptosis rate was increased with the increased concentration of H2O2,and the concentration of 300 μmol/L.H2O2 not only significantly induced the cell apoptosis but also inhibited compared with control group,H2O2 could inhibit the expression of Bcl-2.Compared with H2O2 group,treatment of TSG improved the rate of cell proliferation,inhibited cell apoptosis,and up-regulated the expression of Bcl-2 significantly（P0.01）.Conclusion TSG inhibited H2O2-induced apoptosis of human umbilical vein endothelial cells,which might be associated with the increase of Bcl-2 expression.