安普克
血管紧张素II
化学
磷酸化
氧化应激
蛋白激酶A
基因沉默
细胞生物学
肾素-血管紧张素系统
信号转导
内科学
内分泌学
血管紧张素受体
受体
生物
生物化学
医学
基因
血压
作者
Shengyuan Xiao,Yuying Ma,J Li,Y Zhang,Huimin He,Ching‐Ju Fang,W Wang
出处
期刊:PubMed
日期:2021-03-25
卷期号:41 (3): 384-390
标识
DOI:10.12122/j.issn.1673-4254.2021.03.10
摘要
To investigate the mechanism by which angiotensin Ⅱ-induced oxidative stress response inhibits AMPK/ SIRT1 signaling in RAW264.7 macrophages.RAW264.7 cells were treated with 0.5, 1, 3, 10, or 20 μmol/L angiotensin Ⅱ for 24 h, and the changes in the expressions of AMPK, p-AMPK, and SIRT1 proteins were detected using Western blotting. The intracellular ROS release level was measured and the levels of SOD and MDA were detected. The effects of angiotensin Ⅱ type 1 receptor (AT1R) gene silencing on the cell response to angiotensin Ⅱ treatment were examined by detecting the changes in AMPK, p-AMPK and SIRT1 protein levels. The effects of a ROS inhibitor on cellular AMPK and SIRT1 were also examined.Angiotensin Ⅱ stimulation at 20 μmol/L significantly inhibited the phosphorylation of AMPK protein and increased cellular ROS release (P < 0.05). Treatment with 0.5-10 μmol/L angiotensin Ⅱ did not cause significant changes in SOD activity or MDA expression, but angiotensin Ⅱ at the dose of 20 μmol/L significantly inhibited SOD activity in the cells (P < 0.05). In the macrophages with AT1R gene silencing, treatment with angiotensin Ⅱ did not obviously inhibit AMPK phosphorylation or down- regulate SIRT1 expression. In cells treated with the ROS inhibitor, angiotensin Ⅱ failed to lower the level of AMPK phosphorylation or the expression of SIRT1.Angiotensin Ⅱ induces oxidative stress to cause disturbance of AMPK/ SIRT1 signaling pathway in macrophages.
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