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

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Activation of alpha-7 nicotinic acetylcholine receptors suppresses inflammation and endometriotic lesion development in a mouse model by reducing IL-1β expression.

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Abstract

OBJECTIVE: We investigated α-7 nAchR expression in human peritoneal macrophages and examined whether activation of nAchR 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.

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Condition tags

endometriosis

MeSH descriptors

Aconitine alpha7 Nicotinic Acetylcholine Receptor Bridged Bicyclo Compounds, Heterocyclic Endometriosis Macrophages, Peritoneal Quinuclidines RNA, Messenger Aconitine Aconitine Adult alpha7 Nicotinic Acetylcholine Receptor alpha7 Nicotinic Acetylcholine Receptor alpha7 Nicotinic Acetylcholine Receptor alpha7 Nicotinic Acetylcholine Receptor Animals Ascitic Fluid Ascitic Fluid Ascitic Fluid Bridged Bicyclo Compounds, Heterocyclic Bridged Bicyclo Compounds, Heterocyclic

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