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

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