中文摘要：

目的观察二苯乙烯苷干预过氧化氢致人脐静脉内皮细胞凋亡及对凋亡调控蛋白Bcl-2和Bax表达的影响。方法体外培养人脐静脉内皮细胞，实验分为对照组、300μmol／L过氧化氢组及二苯乙烯苷预处理组，采用MTT法、形态学观察、流式细胞仪检测内皮细胞凋亡情况，Western blot检测二苯乙烯苷对Bcl-2和Bax表达的影响。结果内皮细胞经过氧化氢处理后，其增殖明显受到抑制，凋亡率显著升高，Bcl-2蛋白表达减少，Bax蛋白表达显著增加，Bcl-2／Bax比值降低，差异均有显著性（P〈0．01）；经二苯乙烯苷预处理后，细胞增殖率显著提高，凋亡率显著降低；Bcl-2蛋白表达增加，Bax蛋白表达减少，Bcl-2／Bax比值明显提高，差异均有显著性（P〈0．01）。结论二苯乙烯苷可通过调节Bcl-2／Bax表达而抑制过氧化氢诱导的人脐静脉内皮细胞凋亡，减少内皮细胞损伤。

英文摘要：

Aim To investigate the effects of tetrahydroxystilbene-2-O-β-D- glucoside （TSG） on the apoptosis of human umbilical vein endothelial cells （HUVEC） and its molecular mechanisms induced by hydrogen peroxide （ H2 02 ）. Methods The model of apoptosis HUVEC was induced by 300 μmol/L H202, MTT assay was used to detect the cell proliferation, flowing cytometry was used to measure the effect of apoptosis. The expression of Bcl-2 and Bax was detected by Western blot. Results H202 could inhibit the viability of cells, decrease the expression of Bcl-2 and the ratio of Bcl-2/ Bax, and increase the apoptosis ratio and the expression of Bax. On the contrary, treatment of TSG could improve the rate of cell proliferation, inhibit cell apoptosis, up-regulate the expression of Bcl-2 and increase the ratio of Bcl-2/Bax, down-reg- ulate the expression of Bax significantly （P 〈 0. 01 ）. Conclusions TSG could inhibit H2 02-induced apoptosis of HU- VEC, and the mechanisms might be associated with regulating the expression of Bcl-2, Bax and the ratio of Bcl-2/Bax.