氧化应激
安普克
线粒体生物发生
内皮功能障碍
线粒体
西妥因1
氧化磷酸化
化学
线粒体ROS
SIRT3
药理学
内分泌学
细胞生物学
内科学
生物
医学
乙酰化
生物化学
下调和上调
磷酸化
蛋白激酶A
锡尔图因
基因
作者
Kun Ling Tsai,Ching Hsia Hung,Shih Hung Chan,Pei‐Ling Hsieh,Hsiu Chung Ou,Yung Hsin Cheng,Pei Ming Chu
标识
DOI:10.1002/mnfr.201700928
摘要
Scope Endothelial dysfunction is an important mechanism in the development of atherosclerosis and is thought to be critical for predicting cardiovascular diseases. Previous reports suggested that chlorogenic acid (CGA) is a potent antioxidant and anti‐inflammatory compound. The molecular mechanisms underlying the inhibitory effects of CGA on oxLDL‐induced oxidative injuries in human endothelial cells are still largely unknown. This study is aimed to test the hypothesis that CGA protects against oxLDL‐facilitated oxidative stress by upregulating SIRT1 and to explore the role of AMPK/PGC‐1 pathway and mitochondrial biogenesis. Methods and results HUVECs were treated with oxLDL in the presence or absence of CGA pretreatment. Our data indicated that CGA pretreatment increased SIRT1 deacetylase activity levels. In addition, CGA reversed oxLDL‐impaired SIRT1 and AMPK/PGC‐1 activity and mitigated oxLDL‐induced oxidative stress and dysfunction of mitochondrial biogenesis. However, silencing SIRT1, AMPK, and PGC‐1 abated the ability of CGA to protect against oxidative stress. Results from the present study also suggested that CGA inhibits oxLDL‐induced endothelial apoptosis through modulating SIRT1 and AMPK/PGC‐1 function. Conclusion These findings provide new insights into possible molecular mechanisms by which CGA mitigates oxLDL‐induced endothelial oxidative stress and mitochondrial dysfunction by activating SIRT1 and modulating the AMPK/PGC‐1 signaling pathway.
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