title: [Anti-atherosclerosis role of N-oleoylethanolamine in CB2].
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.
authors: Ya-Ting
authors: YT
authors: Gai
authors: Qiang
authors: Q
authors: Shu
authors: Cai-Xia
authors: CX
authors: Chen
authors: You-Lin
authors: YL
authors: Lai
authors: Wen-Jun
authors: WJ
authors: Li
authors: Lu
authors: L
authors: Peng
authors: Li-Min
authors: LM
authors: Lin
authors: Xin
authors: X
authors: Jin
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D050197:Atherosclerosis / Q000473:pathology*; D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D063388:Endocannabinoids / Q000494:pharmacology*; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism*; D004983:Ethanolamines / Q000494:pharmacology*; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects; D009829:Oleic Acids / Q000494:pharmacology*; D047493:PPAR alpha / Q000037:antagonists & inhibitors; D012333:RNA, Messenger / Q000378:metabolism; D043885:Receptor, Cannabinoid, CB2 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D002722:Chlorobenzenes
chemical_list: D000893:Anti-Inflammatory Agents; D063388:Endocannabinoids; D004983:Ethanolamines; D007211:Indoles; D009829:Oleic Acids; D047493:PPAR alpha; D012333:RNA, Messenger; D043885:Receptor, Cannabinoid, CB2; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; C060893:MK-886; D002722:Chlorobenzenes; C033595:N-oleoylethanolamine; C094023:iodopravadoline