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目的研究赛格列酮对血管紧张素Ⅱ诱导人脐静脉内皮细胞表达细胞间粘附分子1和血管细胞粘附分子1上调的影响。方法以不同浓度的赛格列酮(0.1μmol/L、1μmol/L1、0μmol/L和100μmol/L)预处理人脐静脉内皮细胞24 h,再与10-7mmol/L血管紧张素Ⅱ共孵育12 h。通过半定量逆转录聚合酶链反应和Western Blot分别检测细胞间粘附分子1和血管细胞粘附分子1 mRNA和蛋白表达的情况。结果与血管紧张素Ⅱ组相比,0.1μmol/L和1μmol/L赛格列酮预处理24 h组对血管紧张素Ⅱ诱导人脐静脉内皮细胞表达细胞间粘附分子1 mRNA上调无抑制作用(1.107±0.091比1.104±0.081和1.062±0.051,P>0.05),而10μmol/L和100μmol/L组则有明显的抑制作用(0.814±0.016和0.766±0.026,P<0.01和P<0.001);细胞间粘附分子1蛋白表达分别下调52.9%和55.5%(P<0.01和P<0.001)。而不同浓度的赛格列酮(0.1μmol/L、1μmol/L、10μmol/L和100μmol/L)使血管细胞粘附分子mRNA表达分别下调14.2%、19.5%、45.1%和60.7%(0.1μmol/L时P<0.01,余P<0.001);蛋白表达分别下调17.8%、33.8%、54.5%和58.9%(0.1μmol/L时P<0.01,余P<0.001)。结论赛格列酮抑制血管紧张素Ⅱ上调人脐静脉内皮细胞表达血管细胞粘附分子1,并呈浓度依赖效应;但对细胞间粘附分子1无论是mRNA还是蛋白水平,在低浓度(0.1μmol/L和1μmol/L)时无抑制作用,在较高浓度(10μmol/L和100μmol/L)可有较明显的抑制作用。
Objective To investigate the effects of glitazone on the upregulation of the expression of intercellular adhesion molecule - 1 and vascular cell adhesion molecule 1 induced by angiotensin Ⅱ in human umbilical vein endothelial cells. Methods Human umbilical vein endothelial cells were pretreated with different concentrations of Soglitazone (0.1μmol / L, 1μmol / L, 0μmol / L and 100μmol / L) for 24 hours and incubated with 10-7mmol / L Angiotensin Ⅱ 12 h. Semi-quantitative reverse transcriptase-polymerase chain reaction and Western Blot were used to detect the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 mRNA and protein, respectively. Results Compared with angiotensin Ⅱ group, pretreatment with 0.1 μmol / L and 1 μmol / L Soglitazone for 24 h had no effect on angiotensin Ⅱ - induced up - regulation of intercellular adhesion molecule - 1 mRNA expression in human umbilical vein endothelial cells (1.107 ± 0.091 vs 1.104 ± 0.081 and 1.062 ± 0.051, P> 0.05), while 10μmol / L and 100μmol / L groups showed significant inhibition (0.814 ± 0.016 and 0.766 ± 0.026, P <0.01 and P <0.001) ; The expression of intercellular adhesion molecule-1 was down-regulated by 52.9% and 55.5% (P <0.01 and P <0.001), respectively. However, the mRNA expressions of vascular cell adhesion molecules were down-regulated by 14.2%, 19.5%, 45.1% and 60.7% (0.1μmol / L, 0.1μmol / L and 1μmol / L, 10μmol / L and 100μmol / / L, P <0.01, P <0.001). The protein expression was down-regulated by 17.8%, 33.8%, 54.5% and 58.9% (P <0.01, P <0.001; Conclusions Slitogrel inhibits the up-regulation of angiotensin II by up-regulating the expression of vascular cell adhesion molecule-1 in a concentration-dependent manner in human umbilical vein endothelial cells. However, at a low concentration of 0.1 μmol / L and 1μmol / L), and inhibited the proliferation at higher concentrations (10μmol / L and 100μmol / L).