Bornyl acetate suppresses ox-LDL-induced attachment of THP-1 monocytes to endothelial cells

Biomed Pharmacother. 2018 Jul:103:234-239. doi: 10.1016/j.biopha.2018.03.152. Epub 2018 Apr 24.

Abstract

Leukocyte recruitment to the surface of the endothelium plays a pivotal role in the development of cardiovascular diseases. Bornyl acetate is the main volatile constituent present in numerous conifer oils, which has displayed its anti-oxidant and anti-inflammatory properties in different types of tissues and cells. However, little information regarding the effects of bornyl acetate on vascular endothelial inflammation has been reported before. In the current study, we aimed to investigate the pharmacological roles of bornyl acetate against ox-LDL-induced leukocyte adhesion to the endothelium. Our findings indicate that bornyl acetate ameliorated ox-LDL-induced reduction in cell viability of HUVECs. Additionally, bornyl acetate inhibited the attachment of THP-1 monocytes to HUVECs induced by treatment with ox-LDL through ameliorating the expression of ICAM-1, VCAM-1, and E-selectin. Mechanistically, we found that bornyl acetate could suppress activation of the IκBα/NF-κB signaling pathway. Lastly, our results indicate that bornyl acetate mitigated expression of the pro-inflammatory cytokines TNF-α and IL-1β. Our results suggest the therapeutic potential of bornyl acetate in patients with atherosclerosis.

Keywords: Atherosclerosis; Bornyl acetate; Endothelium; NF-κB; ox-LDL.

MeSH terms

  • Camphanes / pharmacology*
  • Cell Adhesion / drug effects
  • Cell Adhesion Molecules / metabolism
  • Cell Survival / drug effects
  • Human Umbilical Vein Endothelial Cells / cytology*
  • Human Umbilical Vein Endothelial Cells / drug effects
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Humans
  • Interleukin-1beta / metabolism
  • Lipoproteins, LDL / pharmacology*
  • Monocytes / cytology*
  • Monocytes / drug effects
  • Monocytes / metabolism
  • NF-KappaB Inhibitor alpha / metabolism
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Phosphorylation / drug effects
  • Promoter Regions, Genetic / genetics
  • Transcription, Genetic / drug effects
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Camphanes
  • Cell Adhesion Molecules
  • Interleukin-1beta
  • Lipoproteins, LDL
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • oxidized low density lipoprotein
  • NF-KappaB Inhibitor alpha
  • bornyl acetate