2. Academic Validation
  3. Ginsenoside F1 Ameliorates Endothelial Cell Inflammatory Injury and Prevents Atherosclerosis in Mice through A20-Mediated Suppression of NF-kB Signaling

Ginsenoside F1 Ameliorates Endothelial Cell Inflammatory Injury and Prevents Atherosclerosis in Mice through A20-Mediated Suppression of NF-kB Signaling

  • Front Pharmacol. 2017 Dec 22;8:953. doi: 10.3389/fphar.2017.00953.
Meng Qin 1 2 3 4,  Yun Luo 1 2 3 4,  Shan Lu 1 2 3 4,  Jing Sun 5,  Ke Yang 6,  Guibo Sun 1 2 3 4,  Xiaobo Sun 1 2 3 4
Affiliations

Affiliations

  • 1 Institute of Medicinal Plant Development, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
  • 2 Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
  • 3 Key Laboratory of Bioactive Substances and Resource Utilization of Chinese Herbal Medicine, Ministry of Education, Beijing, China.
  • 4 Key Laboratory of Efficacy Evaluation of Chinese Medicine against Glyeolipid Metabolism Disorder Disease, State Administration of Traditional Chinese Medicine, Beijing, China.
  • 5 Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China.
  • 6 Collaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, Zhejiang University of Technology, Hangzhou, China.
PMID: 29311947 DOI: 10.3389/fphar.2017.00953
Abstract

Atherosclerosis (AS) is a chronic inflammatory disease and endothelial cell injury is the initial event. In this study, we investigated the protective effects of ginsenoside F1 (GF1) on AS and the potential molecular mechanisms of ox-LDL induced endothelial injury. ApoE-/- mice were fed a high fat diet and orally treated with GF1 (50 mg/kg/day) for 8 weeks. Atherosclerotic plaque and LOX-1, TLR4, NF-κB expression levels in the aortic root and inflammatory factor MPO in whole body were measured. The treatment with GF1 induced a remarkable reduction in the atherosclerotic lesion area, LOX-1, TLR4 expression and decreased the MPO distribution. Meanwhile, in vitro study, we confirmed that GF1 treatment greatly increased ox-LDL-injured endothelial cell viability, ameliorated LOX-1, TLR4 expression levels and reduced monocytes adhesion. Protein microarray demonstrated that GF1 significantly inhibited G-CSF, ICAM-1, MIP-1δ, IL-1α, IL-15, IL-16 levels. Mechanistically, the GF1 treatment suppressed the NF-κB nuclear translocation. Furthermore, our data indicated that GF1 significantly increased A20 expression level and A20 siRNA markedly abolished the attenuation of GF1 on NF-κB nuclear translocation and inflammatory factors expression. Our results suggest that the GF1 may be a potential drug for anti-atherosclerosis.

Keywords

A20; Ginsenoside F1; HUVECs; atherosclerosis; inflammatory injury; ox-LDL.

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