Related Experiment Video
Updated: Dec 22, 2025

08:15
Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
845
Ginsenoside Rb1 reduces H2O2‑induced HUVEC dysfunction by stimulating the sirtuin‑1/AMP‑activated protein kinase
Zhenda Zheng1, Min Wang1, Cailian Cheng2
1Department of Cardiology, The Third Affiliated Hospital of Sun Yat‑sen University, Sun Yat‑sen University, Guangzhou, Guangdong 510630, P.R. China.
Molecular Medicine Reports
|May 8, 2020
Summary
Ginsenoside Rb1 protects against endothelial cell aging by activating SIRT1 and AMPK. This pathway enhances nitric oxide production and reduces aging markers, offering insights into cardiovascular disease prevention.
Area of Science:
- Cardiovascular Biology
- Cellular Aging Mechanisms
- Pharmacology of Ginseng
Background:
- Endothelial dysfunction and senescence are key factors in cardiovascular diseases like atherosclerosis and hypertension.
- Ginsenoside Rb1 (Rb1), a ginseng compound, shows anti-obesity and anti-inflammatory effects.
- Previous studies indicated Rb1 activates Sirtuin-1 (SIRT1) to protect against hydrogen peroxide (H2O2)-induced human umbilical vein endothelial cell (HUVEC) aging.
Purpose of the Study:
- To investigate the role of AMP-activated protein kinase (AMPK) in the SIRT1 signaling pathway during H2O2-induced HUVEC aging.
- To elucidate the molecular mechanisms by which Rb1 protects HUVECs from senescence via the SIRT1/AMPK pathway.
Main Methods:
- Induction of HUVEC aging using H2O2.
- Treatment with Ginsenoside Rb1 (Rb1).
- Inhibition of AMPK using compound C and SIRT1 using nicotinamide.
- Assessment of SIRT1 expression, AMPK phosphorylation, endothelial nitric oxide synthase (eNOS) expression, nitric oxide (NO) production, and PAI-1 expression.
Main Results:
- Rb1 restored H2O2-induced reduction in SIRT1 expression and activated AMPK phosphorylation.
- Rb1-induced AMPK activation increased eNOS expression and NO production, while suppressing PAI-1 expression.
- Inhibition of AMPK or SIRT1 abrogated the protective effects of Rb1 against H2O2-induced endothelial aging.
Conclusions:
- Rb1 protects against H2O2-induced HUVEC senescence.
- The protective mechanism involves the activation of the SIRT1/AMPK signaling pathway.
- This study provides novel insights into the molecular basis of Rb1's cardioprotective effects.

