论文部分内容阅读
目的 生理水平的血流剪切应力有抑制内皮细胞凋亡等作用 ,进而发挥抗动脉粥样硬化作用 ,本研究的目的是阐明血流剪切应力抑制血管内皮细胞凋亡的分子机制。方法 人脐静脉内皮细胞培养于DMEM培养液 ,当细胞融合时将细胞暴露于 2 0dyne·cm-2 的剪切应力 ,分别用免疫印迹杂交及实时聚合酶链反应法检测凋亡蛋白X连锁抑制物 (X linkedinhibitorofapoptosisprotein ,XIAP)mRNA及蛋白的表达。结果 2 0dyne·cm-2 的剪切应力刺激 1～ 4h ,可诱导内皮细胞产生XIAPmRNA ,4h时表达最多。 2 0dyne·cm-2 剪切应力刺激 6,1 2和 2 4h ,XI AP蛋白表达明显增加。结论 生理水平的剪切应力明显诱导内皮细胞XIAPmRNA和蛋白的表达 ,这可能是剪切应力抑制内皮细胞凋亡 ,发挥抗动脉粥样硬化作用的机制之一
Purpose Physiological level of shear stress in blood flow can inhibit endothelial cell apoptosis and further exert anti-atherosclerotic effects. The purpose of this study is to elucidate the molecular mechanism by which shear stress in bloodstream inhibits apoptosis of vascular endothelial cells. Methods Human umbilical vein endothelial cells were cultured in DMEM medium. When the cells were fused, the cells were exposed to the shearing stress of 20 dyne · cm-2. Western blotting and real-time polymerase chain reaction were used to detect apoptosis protein X-linked inhibition (X linkedinhibitorofapoptosisprotein, XIAP) mRNA and protein expression. Results Shear stress of 20dyne · cm-2 stimulated for 1 ~ 4h and induced the production of XIAP mRNA in endothelial cells, which was the highest at 4h. The expression of XIAP protein was significantly increased after 6, 12 and 24 hours of 20 dyne · cm-2 shear stress. Conclusion Physiological shear stress induces the expression of XIAP mRNA and protein in endothelial cells, which may be one of the mechanisms by which shear stress inhibits endothelial cell apoptosis and exerts anti-atherosclerotic effects