Ginsenoside Rb2 Ameliorates LPS-Induced Inflammation and ER Stress in HUVECs and THP-1 Cells via the AMPK-Mediated Pathway

Sun J. L., Abd El-Aty A. M., Jeong J. H., Jung T. W.

American Journal of Chinese Medicine, cilt.48, sa.4, ss.967-985, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 48 Sayı: 4
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1142/s0192415x20500469
  • Dergi Adı: American Journal of Chinese Medicine
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, CINAHL, EMBASE, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.967-985
  • Anahtar Kelimeler: Ginsenoside, Rb2, Inflammation, Apoptosis, Atherosclerosis, AMPK, HO-1, ENDOPLASMIC-RETICULUM STRESS, OXYGENASE-1 GENE-EXPRESSION, HEME OXYGENASE-1, INSULIN-RESISTANCE, OXIDATIVE STRESS, COMPOUND K, ACTIVATION, KINASE, INHIBITION, GPR120
  • Atatürk Üniversitesi Adresli: Evet

Özet

© 2020 World Scientific Publishing Company.Inflammation and endoplasmic reticulum (ER) stress have been documented to contribute to the development of atherosclerosis. Ginsenoside Rb2 has been reported to exhibit antidiabetic effects. However, the effects of Rb2 on atherosclerotic responses such as inflammation and ER stress in endothelial cells and monocytes remain unclear. In this study, the expression of inflammation and ER stress markers was determined using a Western blotting method. Concentrations of tumor necrosis factor alpha (TNFα) and monocyte chemoattractant protein-1 (MCP-1) in culture media were assessed by enzyme-linked immunosorbent assay (ELISA) and apoptosis was evaluated by a cell viability assay and a caspase-3 activity measurement kit. We found that exposure of HUVECs and THP-1 monocytes to Rb2 attenuated inflammation and ER stress, resulting in amelioration of apoptosis and THP-1 cell adhesion to HUVECs under lipopolysaccharide (LPS) condition. Increased AMPK phosphorylation and heme oxygenase (HO)-1 expression, including GPR120 expression were observed in Rb2-treated HUVECs and THP-1 monocytes. Downregulation of both, AMPK phosphorylation and HO-1expression rescued these observed changes. Furthermore, GPR120 siRNA mitigated Rb2-induced AMPK phosphorylation. These results suggest that Rb2 inhibits LPS-mediated apoptosis and THP-1 cell adhesion to HUVECs by GPR120/AMPK/HO-1-associated attenuating inflammation and ER stress. Therefore, Rb2 can be used as a potential therapeutic molecule for treatment of atherosclerosis.