We have located links that may give you full text access.
N-Oleoylethanolamine Reduces Inflammatory Cytokines and Adhesion Molecules in TNF-α-induced Human Umbilical Vein Endothelial Cells by Activating CB2 and PPAR-α.
Journal of Cardiovascular Pharmacology 2016 October
Inflammation plays a pivotal role in the pathogenesis of atherosclerosis. Peroxisome proliferator-activated receptor-alpha (PPAR-α) and cannabinoid receptor 2 (CB2) crucially impact the modulation of inflammation. N-Oleoylethanolamine (OEA), a natural agonist of PPAR-α, can also up-regulate the expression of CB2 in human umbilical vein endothelial cells (HUVECs) and further shows an antiatherosclerotic effect. Our study was designed to determinate whether OEA could inhibit inflammation in HUVECs induced by tumor necrosis factor-α (TNF-α) and to identify the mechanism of OEA function. Interleukin-6 (IL-6), interleukin-8 (IL-8), vascular adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) levels were detected in HUVECs exposed to tumor necrosis factor-α in the presence of OEA. The results showed that OEA suppressed the expression of interleukin-6, interleukin-8, vascular adhesion molecule-1, and intercellular adhesion molecule-1 in a dose-dependent manner. OEA also enhanced CB2 and PPAR-α receptor expression, which contributed to its anti-inflammatory effect. OEA inhibited the nuclear factor-κB (NF-κB) pathway, and the effect of OEA on nuclear factor-κB was partly abolished when HUVECs were pretreated with either CB2 or PPAR-α antagonist. OEA attenuated tumor necrosis factor-α-induced inflammation in HUVECs by up-regulating the expression of CB2 and PPAR-α receptors. Furthermore, OEA suppresses the nuclear factor-κB pathway. These results suggest that OEA exerts anti-inflammatory and anti-adhesive effects on HUVECs.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app