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目的研究血管紧张素Ⅱ(AngⅡ)和血管紧张素转换酶抑制剂(ACEI),卡托普利和AngⅡ1型受体(AT-1)拮抗剂缬沙坦对人脐静脉内皮细胞(HUVECs)1型纤溶酶原激活物抑制剂(PAI-1)、组织型纤溶酶原激活剂(tPA)蛋白的释放及活性的影响。方法将不同浓度的AngⅡ(10-6~10-9mol/L)与HUVECs共同孵育24h,以及将10-6mol/L的AngⅡ与HUVECs作用不同时间(0、4、8、12、24h)后,用细胞酶联免疫法和发色底物法分别检测细胞培养液中PAI-1、tPA的含量及活性,并观察卡托普利和缬沙坦干预后的影响。结果10-6mol/LAngⅡ作用HUVECs24h后,可使细胞分泌的PAI-1含量与对照组相比明显增高(280±15.60vs83.33±10.56)ng/mL,P<0.01),PAI-1活性明显增加(9.25±0.39vs7.53±0.33)IU/mL,P<0.01),AngⅡ虽也可刺激tPA含量增加(101.67±3.78vs70±5.62)ng/mL,(P<0.01),但PAI-1的增量是tPA增量的6~7倍(Δ196.67±21.34vsΔ31±6.50)ng/mL,(P<0.01),AngⅡ对tPA活性无影响(0.97±0.05vs0.95±0.08)ng/mL,(P>0.05);缬沙坦可显著抑制AngⅡ的促PAI-1分泌作用(212.67±5.38vs290±6.57)IU/mL,(P<0.01),而卡托普利对AngⅡ的促PAI-1分泌作用无明显抑制作用(278.33±9.16vs290±6.57)IU/mL,(P>0.05)。结论AngⅡ可促使HUVECs分泌PAI-1,并使其活性增加;AngⅡ亦可刺激tPA分泌,但作用弱于PAI-1,对其活性无明显影响。缬沙坦可抑制AngⅡ促HUVECs分泌PAI-1的作用;卡托普利的作用不显著。
Objective To investigate the effects of angiotensin Ⅱ (AngⅡ) and angiotensin converting enzyme inhibitor (ACEI), captopril and angiotensin Ⅱ type 1 receptor (AT-1) antagonist valsartan on human umbilical vein endothelial cells (HUVECs) Effect of plasminogen activator inhibitor (PAI-1), tissue plasminogen activator (tPA) release and activity. Methods Ang Ⅱ (10-6 ~ 10-9mol / L) and HUVECs were incubated with HUVECs at different concentrations for 24 hours, and incubated with HUVECs at a dose of 10-6mol / L for different time (0,4,8,12,24 h) The contents and activities of PAI-1 and tPA in cell culture medium were detected by enzyme-linked immunosorbent assay (ELISA) and chromogenic substrate method respectively. The effects of captopril and valsartan were also observed. Results After treated with 10-6mol / LAngⅡ for 24h, the PAI-1 secretion of HUVECs was significantly higher than that of the control group (280 ± 15.60 vs 83.33 ± 10.56) ng / mL, P <0.01) (9.25 ± 0.39vs7.53 ± 0.33) IU / mL, P <0.01). Although Ang II could stimulate the increase of tPA level (101.67 ± 3.78vs70 ± 5.62) ng / mL, (P <0.01). AngⅡ had no effect on tPA activity (0.97 ± 0.05 vs0.95 ± 0.08 ng / mL, mL, P <0.05). Valsartan significantly inhibited AngⅡ-induced PAI-1 secretion (212.67 ± 5.38 vs 290 ± 6.57) IU / mL, (P <0.01) -1 secretion had no significant inhibitory effect (278.33 ± 9.16 vs 290 ± 6.57) IU / mL, (P> 0.05). Conclusions Ang Ⅱ can induce the secretion of PAI-1 from HUVECs and increase its activity. AngⅡ also stimulates the secretion of tPA, but its effect is weaker than that of PAI-1, and has no significant effect on its activity. Valsartan can inhibit Ang Ⅱ promote the secretion of PAI-1 HUVECs role; Captopril effect was not significant.