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目的探讨17β-雌二醇(17β-estradiol,E2)对于血管内皮细胞中血管细胞黏附分子1(VCAM-1)的表达影响,探索miR-126在其中的作用。方法培养人脐静脉血管内皮细胞,以脂多糖LPS刺激诱导炎症反应,给予不同浓度梯度的E2处理不同时间,应用免疫印迹法观察VCAM-1的蛋白表达。转染miR-126的抑制物沉默miR-126表达后,观察E2对VCAM-1蛋白表达的影响变化。结果与对照组比较,LPS可诱导VCAM-1蛋白表达增加(854.0±21.3)%,n=3,P<0.01)。分别给予不同浓度的E2(10-8~10-6 mol/L)预处理后,均能抑制VCAM-1蛋白表达。抑制率分别为(44.3±4.0)%(n=3,P<0.05)、(45.1±7.1)%(n=3,P<0.05)和(65.9±7.2)%(n=3,P<0.01);E2(10-8 mol/L)分别处理内皮细胞24、48、72h后,可呈时间依赖性抑制LPS所诱导的VCAM-1的蛋白表达,抑制率分别为(52.1±4.4)%、(59.5±7.7)%和(64.5±6.5)%(n=3,P<0.05)。转染miR-126的抑制物可明显抑制miR-126表达[抑制率为(75.8±6.7)%,n=3,P<0.01],该抑制物可明显抑制17β-雌二醇对VCAM-1蛋白的抑制作用。结论 E2通过miR-126下调LPS诱导的血管内皮细胞VCAM-1蛋白表达。
Objective To investigate the effect of 17β-estradiol (E2) on the expression of vascular cell adhesion molecule 1 (VCAM-1) in vascular endothelial cells and explore the role of miR-126 in it. Methods Human umbilical vein endothelial cells were cultured and stimulated by lipopolysaccharide (LPS). The inflammatory response was induced by lipopolysaccharide (LPS). Different concentrations of E2 were treated for different time. Western blotting was used to observe the protein expression of VCAM-1. Inhibition of miR-126 silencing miR-126 expression, observed E2 on VCAM-1 protein expression changes. Results Compared with the control group, LPS induced an increase of VCAM-1 protein expression (854.0 ± 21.3%), n = 3, P <0.01). After pretreatment with different concentrations of E2 (10-8 ~ 10-6 mol / L), the expression of VCAM-1 protein was inhibited. The inhibitory rates were (45.3 ± 7.1)% (n = 3, P <0.05) and (65.9 ± 7.2)% (n = 3, P <0.01) ) E2 (10-8 mol / L) for 24,48 and 72 h, respectively, inhibited the protein expression of VCAM-1 induced by LPS in a time-dependent manner, with the inhibition rates of 52.1 ± 4.4% (59.5 ± 7.7)% and (64.5 ± 6.5)%, respectively (n = 3, P <0.05). Inhibition of miR-126 by miR-126 could significantly inhibit the expression of miR-126 [(75.8 ± 6.7)%, n = 3, P <0.01] Inhibition of protein. Conclusion E2 down-regulates LPS-induced VCAM-1 protein expression in vascular endothelial cells by miR-126.