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

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

  • J Cardiovasc Pharmacol. 2020 Feb;75(2):155-167. doi: 10.1097/FJC.0000000000000775.
Guangyao Shi 1 Dinghui Liu 1 Bin Zhou 1 Yong Liu 1 Baoshun Hao 1 Shujie Yu 1 Lin Wu 1 Min Wang 1 Zhiming Song 2 Chaodong Wu 3 Jieming Zhu 1 Xiaoxian Qian 1 4
Affiliations

Affiliations

  • 1 Department of Cardiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
  • 2 Department of Cardiology, The First Affiliated Hospital of Henan University, Kaifeng, Henan, China.
  • 3 Department of Nutrition and Food Science, Texas A&M University, College Station, TX; and.
  • 4 Institute Integrated Traditional Chinese and Western Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
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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