Original ArticleEffect of Ginsenoside Rh1 on Proliferation, Apoptosis, and Oxidative Stress in Vascular Endothelial Cells by Regulation of the Nuclear Erythroid 2-related Factor-2/Heme Oxygenase-1 Signaling PathwayXu, Hai; Jiang, Yicheng; Yu, Kun; Zhang, Xiwen; Shi, Yafei Author Information Department of Cardiology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, China. Correspondence: Yafei Shi, Department of Cardiology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No. 6 West Rd Beijing, Huaian 223300, China (e-mail: [email protected]). The authors report no conflicts of interest. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. Journal of Cardiovascular Pharmacology: March 2022 - Volume 79 - Issue 3 - p 335-341 doi: 10.1097/FJC.0000000000001121 Buy Metrics Abstract This study aimed to investigate the role of ginsenoside Rh1 in regulating the proliferation, apoptosis, and oxidative stress in oxidized low-density lipoprotein (ox-LDL)-treated human vascular endothelial cells (VECs) and the underlying mechanisms. VECs were treated with ox-LDL to generate an in vitro atherosclerosis model. The effect of ginsenoside Rh1 on cell viability and proliferation was examined by MTT and colony formation assays, respectively, and cell apoptosis was determined by flow cytometry and transferase dUTP nick end-labeling assay. The levels of reactive oxygen species, malondialdehyde, and superoxide dismutase activity were detected using biological assays. Finally, the effect of ginsenoside Rh1 on the levels of BAX and BCL-2 and the nuclear erythroid 2-related factor-2/heme oxygenase (HO)-1 signaling pathway was determined by quantitative real-time polymerase chain reaction and western blot assays. Treatment with ginsenoside Rh1 significantly increased the proliferation and decreased the apoptosis of ox-LDL–treated VECs in a dose-dependent manner. Moreover, ginsenoside Rh1 also relieved oxidative stress in ox-LDL–treated VECs by activating the Nrf2/HO-1 signaling pathway. Thus, ginsenoside Rh1 affects the proliferation, apoptosis, and oxidative stress in ox-LDL–treated VECs by activating the Nrf2/HO-1 signaling pathway. Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc.