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

    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Mas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。

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    AimTo study the effect of angiotensin(1-7) on inhibiting the inflammation induced by angiotensinⅡ (AngⅡ).MethodsCultured 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.ResultsAng(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.ConclusionAng(1-7) effectively represses the phosphorylation of p38MAPK induced by AngⅡ in HUVEC.

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梁长清, 杨志明, 龚鸿裕, 卢万可, 高然, 张娜娜.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[J].中国动脉硬化杂志,2011,19(1):39~43.

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  • 收稿日期:2010-09-07
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