Ginsenoside Rb1 Alleviates Oxidative Low-Density Lipoprotein–Induced Vascular Endothelium Senescence via the SIRT1/Beclin-1/Autophagy Axis

脐静脉 自噬 衰老 高脂血症 西妥因1 内皮 化学 氧化应激 细胞生物学 内分泌学 内科学 生物 生物化学 医学 细胞凋亡 下调和上调 体外 糖尿病 基因
作者
Guangyao Shi,Dinghui Liu,Bin Zhou,Yong Liu,Baoshun Hao,Shujie Yu,Lin Wu,Min Wang,Zhiming Song,Chaodong Wu,Jieming Zhu,Xiaoxian Qian
出处
期刊:Journal of Cardiovascular Pharmacology [Ovid Technologies (Wolters Kluwer)]
卷期号:75 (2): 155-167 被引量:39
标识
DOI:10.1097/fjc.0000000000000775
摘要

Abstract: Oxidative low-density lipoprotein (ox-LDL) induces endothelium senescence and promotes atherosclerosis. Ginsenoside Rb1 (gRb1) has been proved to protect human umbilical vein cells (HUVECs), but its effect on ox-LDL–induced endothelium senescence and the underlying mechanism remains unknown. This study is to explore the involvement of the SIRT1/Beclin-1/autophagy axis in the effect of gRb1 on protecting endothelium against ox-LDL–induced senescence. Hyperlipidemia of Sprague Dawley rats was induced by high-fat diet, and gRb1 was intraperitoneal injected. A senescence model of HUVECs induced by ox-LDL was also established. The results showed that gRb1 alleviated hyperlipidemia-induced endothelium senescence and ox-LDL-induced HUVECs senescence. GRb1 also restored the reductions in SIRT1 and autophagy, which were involved in the anti-senescence effects. Beclin-1 acetylation was reduced, and the correlation between SIRT1 and Beclin-1 was increased by gRb1. Results of our study demonstrated the anti-senescence function of gRb1 against hyperlipidemia in the endothelium, and the underlying mechanism involves the SIRT1/Beclin-1/autophagy axis.
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