血管紧张素-(1-7)对人脐动脉平滑肌细胞p38MAPK通路的抑制作用

摘要

Objective To study the effect of Angiotensin-(1-7) [Ang-(1-7)] on inhibiting the inflammation induced by Angiotensin Ⅱ (Ang Ⅱ).Methods Cultured Human Umbilical Artery Vascular Smooth Muscle Cells(VSMCs) were incubated for 12 h in the presence of Ang-(1-7),Ang Ⅱ and the specific inhibitor of Ang-(1-7),A-779 at different concentrations either separatedly or in combination.The phosphorylation of p38MAPK were determined by Western blotting.Results Ang-(1-7) dose-dependently inhibited the phosphorylation of p38MAPK induced by Ang Ⅱ in VSMCs.The expression of p38MAPK phosphorylation died down markedly at 1000 nmol/L of Ang-(1-7).Pre-treatment with A-779 for 10 min in VSMCs before Ang-(1-7) and Ang Ⅱ used,the expression of p38 MAPK phosphorylation was nonsignificantly changed.Conclusion Ang-(1-7) effectively represses the phosphorylation of p38MAPK induced by Ang Ⅱ in VSMCs.%目的 探讨血管紧张素-(1-7)[Ang-(1-7)]阻断血管紧张素Ⅱ(AngⅡ)致炎作用的可能机制.方法 用DMEM培养基培养血管平滑肌细胞(VSMCs),待细胞生长至80％融合时无血清培养12小时后分为两组:Ⅰ组:对照组、AngⅡ组、Ang-(1-7)组、AngⅡ+Ang-(1-7)组、AngⅡ+ Ang-(1-7)+ A-779组、A-779组；Ⅱ组:对照组、AngⅡ组、AngⅡ+不同浓度Ang-(1-7)组.上述两组作用一定时间后收集细胞,用Western blot方法测定细胞p38丝裂原活化蛋白激酶(p38MAPK)蛋白磷酸化表达.结果 Ang-(1-7)(1000 nmol/L)可拮抗AngⅡ(100 nmol/L)诱导的VSMCs p38MAPK磷酸化表达,且呈剂量依赖性,随着Ang-(1-7)剂量的增加,p38MAPK磷酸化表达逐渐减弱.结论 Ang-(1-7)呈剂量依赖性抑制AngⅡ激活人脐动脉平滑肌细胞p38MAPK通路的作用,从而可能拮抗AngⅡ的致炎作用.