自噬
安普克
PI3K/AKT/mTOR通路
血管生成
细胞凋亡
癌症研究
药理学
心肌梗塞
细胞生长
细胞
化学
医学
细胞生物学
内科学
生物
激酶
生物化学
蛋白激酶A
作者
Jin Qu,Jinzhu Yin,Zhaozheng Liu
出处
期刊:Tissue & Cell
[Elsevier]
日期:2024-05-03
卷期号:88: 102401-102401
被引量:1
标识
DOI:10.1016/j.tice.2024.102401
摘要
Myocardial infarction (MI) is a kind of cardiovascular diseases with high morbidity and mortality. Poricoic acid A (PAA) is the main active substance in Poria cocos, which has been discovered to exhibit an ameliorative role in the progression of many diseases. However, no report has been focused on the regulatory effects of PAA on MI progression. In this study, at first, oxygen glucose deprivation (OGD) treatment was performed in human cardiac microvascular endothelial cells (HCMECs) to mimic MI cell model. Our findings demonstrated that cell proliferation was reduced post OGD treatment, but which was reversed by PAA treatment. Moreover, PAA suppressed cell apoptosis in OGD-triggered HCMEC cells. Next, it revealed that PAA induced autophagy in OGD-treated HCMEC cells through enhancing LC3-II/LC3-I level and reducing P62 level. In addition, PAA strengthened the angiogenesis ability and migration ability in OGD-induced HCMEC cells. Lastly, it was uncovered that PAA modulated the AMPK/mTOR signaling pathway through affecting the p-mTOR/mTOR and p-AMPK/AMPK levels. In conclusion, PAA can promote angiogenesis and myocardial regeneration after MI by inducing autophagy through modulating the AMPK/mTOR pathway. This work suggested that PAA may be a potential and useful drug for MI treatment.
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