安普克
西妥因1
蛋白激酶A
AMP活化蛋白激酶
衰老
细胞生物学
白藜芦醇
化学
一氧化氮
人参
内皮功能障碍
脐静脉
锡尔图因
磷酸化
生物
内分泌学
生物化学
NAD+激酶
下调和上调
医学
酶
病理
体外
替代医学
基因
作者
Zhaohui Zheng,Min Wang,Cailian Cheng,Dinghui Liu,Lin Wu,Jin Zhu,Xiaoxian Qian
出处
期刊:Molecular Medicine Reports
[Spandidos Publications]
日期:2020-04-28
卷期号:22 (1): 247-256
被引量:27
标识
DOI:10.3892/mmr.2020.11096
摘要
Endothelial dysfunction and senescence are closely associated with cardiovascular diseases including atherosclerosis and hypertension. Ginsenoside Rb1 (Rb1), the major active constituent of ginseng, has been investigated intensively because of its anti‑obesity and anti‑inflammatory effects. In a previous study, hydrogen peroxide (H2O2) was applied to induce human umbilical vein endothelial cell (HUVEC) aging. It was demonstrated that Sirtuin‑1 (SIRT1) was activated by Rb1 to protect HUVECs from H2O2‑induced senescence. However, the mechanisms are not fully understood. The present study examined the role of AMP‑activated protein kinase (AMPK), an energy sensor of cellular metabolism, in the signaling pathway of SIRT1 during H2O2‑stimulated HUVEC aging. It was identified that Rb1 restored the H2O2‑induced reduction of SIRT1 expression, which was consistent with our previous study, together with the activation of AMPK phosphorylation. Using compound C, an AMPK inhibitor, the role of AMPK in the protective effect of Rb1 against H2O2‑induced HUVEC senescence was examined. It was identified that the induction of phosphorylated AMPK by Rb1 markedly increased endothelial nitric oxide synthase expression and nitric oxide production, and suppressed PAI‑1 expression, which were abrogated in HUVECs pretreated with compound C. Further experiments demonstrated that nicotinamide, a SIRT1 inhibitor, downregulated the phosphorylation of AMPK and reduced the protective effects of Rb1 against H2O2‑induced endothelial aging. Taken together, these results provide new insights into the possible molecular mechanisms by which Rb1 protects against H2O2‑induced HUVEC senescence via the SIRT1/AMPK pathway.
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