[Anti-atherosclerosis role of N-oleoylethanolamine in CB2]

Yao Xue Xue Bao. 2014 Mar;49(3):316-21.
[Article in Chinese]

Abstract

To observe a PPAR-alpha agonist effect of N-oleoylethanolamine (OEA) on CB2 (cannabinoid receptor 2), an anti-inflammatory receptor in vascular endothelial cell, healthy HUVECs and TNF-alpha induced HUVECs were used to establish a human vascular endothelial cell inflammatory model. Different doses of OEA (10, 50 and 100 micromol x L(-1)) had been given to HUVECs, cultured at 37 degrees C for 7 h and then collected the total protein and total mRNA. CB2 protein expression was detected by Western blotting and CB2 mRNA expression was assayed by real-time PCR. As the results shown, OEA (10 and 50 micromol x L(-1)) could induce the CB2 protein and mRNA expression, but not 100 micromol x L(-1). To detect if anti-inflammation effect of OEA is partly through CB2, CB2 inhibitor AM630 was used to inhibit HUVEC CB2 expression, then the VCAM-1 expression induced by TNF-alpha was detected, or THP-1 adhere to TNF-alpha induced HUVECs was examined. OEA (50 micromol x L(-1)) could inhibit TNF-alpha induced VCAM-1 expression and THP-1 adhere to HUVECs, these effects could be partly inhibited by a CB2 inhibitor AM630. The anti-inflammation effect of OEA is induced by PPAR-alpha and CB2, suggesting that CB2 signaling could be a target for anti-atherosclerosis, OEA have wide effect in anti-inflammation, it may have better therapeutic potential in anti-inflammation in HUVECs, thus achieving anti-atherosclerosis effect.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents / pharmacology*
  • Atherosclerosis / pathology*
  • Cell Adhesion / drug effects
  • Cells, Cultured
  • Endocannabinoids / pharmacology*
  • Endothelial Cells / cytology
  • Endothelial Cells / metabolism*
  • Ethanolamines / pharmacology*
  • Humans
  • Indoles / pharmacology
  • Monocytes / drug effects
  • Oleic Acids / pharmacology*
  • PPAR alpha / antagonists & inhibitors
  • RNA, Messenger / metabolism
  • Receptor, Cannabinoid, CB2 / antagonists & inhibitors
  • Receptor, Cannabinoid, CB2 / genetics
  • Receptor, Cannabinoid, CB2 / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Anti-Inflammatory Agents
  • Endocannabinoids
  • Ethanolamines
  • Indoles
  • Oleic Acids
  • PPAR alpha
  • RNA, Messenger
  • Receptor, Cannabinoid, CB2
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • MK-886
  • N-oleoylethanolamine
  • iodopravadoline