安普克
衰老
蛋白激酶B
西妥因1
血管紧张素II
磷酸化
细胞生物学
化学
祖细胞
生物
人口
药理学
内分泌学
蛋白激酶A
生物化学
干细胞
下调和上调
医学
环境卫生
基因
血压
作者
Jing Yang,Jie Li,Tingting Wei,Jiyan Pang,Yan‐Hua Du
出处
期刊:ACS pharmacology & translational science
[American Chemical Society]
日期:2023-10-10
卷期号:6 (11): 1673-1680
标识
DOI:10.1021/acsptsci.3c00136
摘要
Aging is associated with an increased risk of cardiovascular disease. Previous studies have demonstrated that compound 3 (C3), a derivative of marine compound xyloallenoide A isolated from the mangrove fungus Xylaria sp. (no. 2508), exhibited strong angiogenic activities in zebrafish. In this study, we examined the effects of C3 on the senescence of endothelial progenitor cells isolated from human peripheral blood (hEPCs). The results showed that treatment with angiotensin II (AngII) for 24 h induced hEPC senescence, as demonstrated by increased SA-β-galactosidase staining. Moreover, there is a significant decrease in telomerase activity and cellular viability in AngII-treated hEPCs. These changes in aging hEPCs were greatly recovered by C3 in a dose-dependent manner. Furthermore, C3 significantly restored the AngII-induced decrease of sirtuin type 1 (SIRT1) expression, a well-known antiaging protein. In addition, AngII increased AMP-activated protein kinase (AMPK) phosphorylation and reduced Akt phosphorylation in aging hEPCs, which were also reversed by C3. Importantly, the inhibition of C3 on hEPC senescence and AMPK/Akt dysregulation was significantly attenuated by the SIRT1-specific inhibitor nicotinoyl. These results indicated that C3 protects hEPC against AngII-induced senescence by increasing SIRT1 expression levels and balancing the AMPK/Akt signaling pathway. The inhibition of hEPCs senescence by C3 might protect EPCs against dysfunction induced by pathological factors in the elderly population. C3 may provide a novel drug candidate for the treatment of aging-related disorders.
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