Alpha-7 nicotinic acetylcholine receptor (nAChR) agonist inhibits the development of endometriosis by regulating inflammation

ObjectiveWe investigated -7 nAchR expression in human peritoneal macrophages and examined whether activation of nAchR might be a new therapy for endometriosis. Materials and methodsHuman peritoneal fluid mononuclear cells (PFMC) were stimulated with lipopolysaccharide (LPS) in the presence of -7 nAChR agonists. In a murine endometriosis model, -7 nAChR modulators were administered. ResultsHuman PFMC expressed -7 nAChR at the mRNA and protein levels. Activation of -7 nAChR with its agonists led to significant (P<.01) suppression of LPS-induced interleukin (IL) -1 expression. In a murine endometriosis model, one week after inoculation of endometrium to the peritoneal cavity, -7 nAChR agonist significantly suppressed the expression of IL-1 mRNA (P<.01), which was negated when -7 nAChR antagonist was administered simultaneously. -7 nAChR agonist significantly suppressed the formation of endometriotic lesions, which was reversed with -7 nAChR antagonist. ConclusionActivation of nAChR might be a new candidate for treatment of endometriosis.