Lipoxin A4 depresses inflammation and promotes autophagy via AhR/mTOR/AKT pathway to suppress endometriosis.

Background: Endometriosis is a benign gynecological disease with the feature of estrogen dependence and inflammation. The function of autophagy and the correlation with inflammation were not yet revealed.

Methods: Autophagosomes were detected by transmission electron microscopy.

Effect of interleukin-1β and lipoxin A in human endometriotic stromal cells: Proteomic analysis.

Aim: Lipoxin A (LXA ) can function as an endogenous 'breaking signal' in inflammation and plays an important role in the progression of endometriosis. The proteome responses to interleukin-1β (IL-1β) or LXA in human endometriotic stromal cells (ESC) are not well understood.

Methods: In this study, primary ESC were cultured from ovarian endometriosis tissue.