A20基因在动脉粥样硬化损伤中对内皮细胞的保护作用

目的　探讨A2 0基因抑制氧化型低密度脂蛋白 (oxidizedlowdensitylipoprotein ,oxLDL)诱导内皮细胞凋亡及相关机制。方法　逆转录 聚合酶链反应检测A2 0基因在oxLDL诱导内皮细胞中的表达。DOTAP脂质体转染pCAGGSEHA2 0和pMAMneo于原代培养的脐静脉内皮细胞 ,经G4 18筛选 ,A2 0表达经免疫荧光鉴定。原位末端标记法、原位杂交检测转染前后oxLDL诱导内皮细胞凋亡情况及同型半胱氨酸蛋白酶 (caspase 3)的表达情况。结果　A2 0基因在oxLDL诱导内皮细胞中不表达。oxLDL诱导内皮细胞凋亡达 2 6 % ,A2 0基因能显著抑制oxLDL诱导的内皮细胞凋亡情况及caspase 3的表达。结论　A2 0基因在动脉粥样硬化的防治中可能有一定作用

Protective effect of A20 gene on endothelial cells in atherosclerotic injury

Objective To examine the effectiveness of A20 in inhibiting oxidized low density lipoprotein (oxLDL)-induced endothelial cell apoptosis.Methods The expression of A20 gene in induction of endothelial cells by oxLDL was examined by RT-PCR.With the help of DOTAP liposome,endothelial cells was transfected with pCAGGSEHA20 and pMAMneo.The positive cell clones were selected with G418.The stable transfection and expression of A20 in the endothelial cells were identified by immunofluorescence analysis.The apoptosis and caspase-3 expression in transfected cells and untransfected cells induced by oxLDL were determined by flow cytometry and in situ hybridization.Results A20 gene did not express in endothelial cells induced by oxLDL.A20 gene can inhibit significantly endothelial cell apoptosis and caspase-3 expression induced by oxLDL.Conclusion A20 gene can be helpful to the treatment of arteriosclerosis.