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Protective effect and mechanism of ginsenoside Rg2 on atherosclerosis

  • Qianqian, Xue (Department of Pharmacology, School of Pharmacy, Qingdao University) ;
  • Tao, Yu (Institute for translational medicine, The Affiliated Hospital of Qingdao University) ;
  • Zhibin, Wang (Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University) ;
  • Xiuxiu, Fu (Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University) ;
  • Xiaoxin, Li (Institute for translational medicine, The Affiliated Hospital of Qingdao University) ;
  • Lu, Zou (Institute for translational medicine, The Affiliated Hospital of Qingdao University) ;
  • Min, Li (Institute for translational medicine, The Affiliated Hospital of Qingdao University) ;
  • Jae Youl, Cho (Department of Integrative Biotechnology and Biomedical Institute for Convergence at SKKU (BICS), Sungkyunkwan University) ;
  • Yanyan, Yang (Department of Immunology, Basic Medicine School, Qingdao University)
  • Received : 2021.12.20
  • Accepted : 2022.08.01
  • Published : 2023.03.02

Abstract

Background: Ginsenoside Rg2 (Rg2) has a variety of pharmacological activities and provides benefits during inflammation, cancer, and other diseases. However, there are no reports about the relationship between Rg2 and atherosclerosis. Methods: We used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) to detect the cell viability of Rg2 in vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs). The expression of inflammatory factors in HUVECs and the expression of phenotypic transformation-related marker in VSMCs were detected at mRNA levels. Western blot method was used to detect the expression of inflammation pathways and the expression of phenotypic transformation at the protein levels. The rat carotid balloon injury model was performed to explore the effect of Rg2 on inflammation and phenotypic transformation in vivo. Results: Rg2 decreased the expression of inflammatory factors induced by lipopolysaccharide in HUVECs-without affecting cell viability. These events depend on the blocking regulation of NF-κB and p-ERK signaling pathway. In VSMCs, Rg2 can inhibit the proliferation, migration, and phenotypic transformation of VSMCs induced by platelet derived growth factor-BB (PDGF-BB)-which may contribute to its anti-atherosclerotic role. In rats with carotid balloon injury, Rg2 can reduce intimal proliferation after injury, regulate the inflammatory pathway to reduce inflammatory response, and also suppress the phenotypic transformation of VSMCs. Conclusion: These results suggest that Rg2 can exert its anti-atherosclerotic effect at the cellular level and animal level, which provides a more sufficient basis for ginseng as a functional dietary regulator.

Keywords

Acknowledgement

This work was supported by The National Natural Science Foundation of China (grant no. 81870331), China, and The Qingdao municipal science and technology bureau project (grant no. 21-1-4-rkjk-12-nsh), China.

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