衰老
蛋白激酶B
西妥因1
血管紧张素II
端粒酶
磷酸化
细胞生物学
化学
锡尔图因
祖细胞
生物
氧化应激
药理学
内皮祖细胞
DNA损伤
癌症研究
内分泌学
激酶
信号转导
祖细胞
毒性
自噬
PI3K/AKT/mTOR通路
氧化磷酸化
细胞毒性
活性氧
端粒
活力测定
内科学
内皮
生物化学
干细胞
作者
Jing Yang,Jie Li,Tingting Wei,Jiyan Pang,Yan‐Hua Du
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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