JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Add like
Add dislike
Add to saved papers

Lipoxin A 4 Suppresses IL-1β-Induced Cyclooxygenase-2 Expression Through Inhibition of p38 MAPK Activation in Endometriosis.

Reproductive Sciences 2019 December
Endometriosis is an inflammation-dependent gynecologic disorder. Increased cyclooxygenase-2 (COX-2) expression plays an important role in the development and progression of endometriosis. Lipoxin A4 (LXA4 ) is an endogenous anti-inflammation lipid and showed inhibitory effects on the development of endometriosis; however, the mechanism remains unclear. In this study, the overexpression of COX-2 was observed in ectopic endometrium of endometriosis patients compared to the normal endometrium of controls. Lipoxin A4 efficiently suppressed IL-1β-induced COX-2 protein expression in ectopic endometriotic stromal cells (ESCs) via its receptor, formyl peptide receptor 2/lipoxin A4 receptor (FPR2/ALX). Antagonism of FPR2/ALX eliminated the inhibitory effect by LXA4 . IL-1β induced the activation of mitogen-activated protein kinases (MAPKs), which can promote the expression of COX-2. Pretreatment of ESCs with LXA4 inhibited the phosphorylation of p38 MAPK induced by IL-1β. These findings suggest that inflammation and MAPKs pathways respond for the abnormal expression of COX-2, which can elucidate the pathophysiology of endometriosis. Moreover, LXA4 suppressed IL-1β-induced COX-2 expression through inhibiting the p38 MAPK signaling protein. This research contributes for better understanding of the cellular and biological events of inflammation and anti-inflammation-mediated regulation in endometriosis.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

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 Toggle icon

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