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目的探讨高糖对内皮细胞转分化的影响及其与血管紧张素Ⅱ(ATⅡ)的关系。方法将人主动脉内皮细胞分成正常浓度葡萄糖(NG)组、高糖(HG)组和厄贝沙坦干预(HG+Irb)组。放射免疫法检测细胞上清液中ATⅡ的浓度。共聚焦显微镜观察CD31和成纤维细胞特异蛋白1(FSP1)的双染色结果。Western blot检测FSP1蛋白水平的表达。结果与NG组比,高糖刺激的内皮细胞导致ATⅡ和FSP1表达增加(P<0.05),呈浓度和时间依赖性。共聚焦显微镜可见CD31和FSP1表达重叠,且一些细胞获得纺锤样的改变并失去CD31染色。厄贝沙坦可抑制高糖引起的上述改变(P<0.05)。结论高糖可能通过ATⅡ介导的内皮细胞转分化导致内皮细胞损伤,而厄贝沙坦抑制内皮细胞转分化。
Objective To investigate the effect of high glucose on transdifferentiation of endothelial cells and its relationship with angiotensin Ⅱ (AT Ⅱ). Methods Human aortic endothelial cells were divided into normal glucose group (NG), high glucose (HG) group and irbesartan intervention group (HG + Irb). Radioimmunoassay was used to detect the concentration of ATⅡ in the cell supernatant. Confocal microscope was used to observe the double staining results of CD31 and fibroblast-specific protein 1 (FSP1). Western blot was used to detect the expression of FSP1 protein. Results Compared with NG group, the expression of ATⅡ and FSP1 was increased in high glucose-stimulated endothelial cells (P <0.05) in a concentration- and time-dependent manner. Confocal microscopy showed CD31 and FSP1 expression overlap, and some cells obtained spindle-like changes and lost CD31 staining. Irbesartan can inhibit these changes caused by high glucose (P <0.05). Conclusion High glucose may induce endothelial cell injury through AT Ⅱ -mediated endothelial cell transdifferentiation, whereas irbesartan inhibits endothelial cell transdifferentiation.