血管紧张素(1-7)对血管紧张素Ⅱ激活人脐静脉内皮细胞p38MAPK通路的拮抗作用

The Effect of Angiotensin(1-7) on Phosphorylation of p38 MAP Kinases Induced by AngiotensinⅡ in Human Umbilical Vein Endothelial Cells

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。方法原代培养人脐静脉内皮细胞,取2-5代用于实验。培养细胞随机分两组：Ⅰ组：对照组,AngⅡ组和AngⅡ＋不同浓度Ang（1-7）组;Ⅱ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。用免疫印迹法测定细胞p38MAPK磷酸化表达。培养细胞用RT-PCR法测定Ang（1-7）的特异性受体M as受体的表达。结果 100 nmol/L Ang（1-7）可以拮抗100 nmol/L AngⅡ诱导的人脐静脉内皮细胞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,在1000 nmol/L Ang（1-7）时即有明显减弱。Ang（1-7）受体特异性拮抗剂A-779可显著抑制Ang（1-7）的此作用。结论 Ang（1-7）呈剂量依赖性拮抗AngⅡ激活人脐静脉内皮细胞p38MAPK通路的作用。

Aim To study the effect of angiotensin（1-7） on inhibiting the inflammation induced by angiotensinⅡ（AngⅡ）.Methods Cultured human umbilical vein endothelial cells（HUVEC） were randomly dividied into different groups,then incubated in the presence of Ang（1-7）,AngⅡ and the specific inhibitor of Ang（1-7）,A-779,and so on.The phosphorylation of p38MAPK were determined by Western blot,and the mRNA for the mas receptor were determined by reverse transcriptional PCR. Results Ang（1-7） dose-dependently inhibited the phosphorylation of p38MAPK induced by AngⅡ in HUVECs.The expression of p38MAPK phosphorylation died down markedly at 1 000 nmol/L of Ang（1-7）.Pre-treatment with A-779 for 10 min in HUVEC before Ang（1-7） and AngⅡ used,the expression of p38 MAPK phosphorylation was nonsignificantly changed. Conclusion Ang（1-7） effectively represses the phosphorylation of p38MAPK induced by AngⅡ in HUVEC.