title: Alpha-7 nicotinic acetylcholine receptor (nAChR) agonist inhibits the development of endometriosis by regulating inflammation.
abstract: We investigated α-7 nAchR expression in human peritoneal macrophages and examined whether activation of nAchR might be a new therapy for endometriosis.
  
  
  
  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.
  
  
  
  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.
  
  
  
  Activation of nAChR might be a new candidate for treatment of endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
authors.forename: Kaori
authors.initials: K
authors.lastname: Yamada-Nomoto
authors.affiliation: Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
authors.forename: Osamu
authors.initials: O
authors.lastname: Yoshino
authors.affiliation: Department of Obstetrics and Gynecology, University of Tokyo, Tokyo, Japan.
authors.forename: Ikumi
authors.initials: I
authors.lastname: Akiyama
authors.affiliation: Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
authors.forename: Akemi
authors.initials: A
authors.lastname: Ushijima
authors.affiliation: Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Ono
authors.affiliation: Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Shima
authors.affiliation: Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
authors.forename: Akitoshi
authors.initials: A
authors.lastname: Nakashima
authors.affiliation: Division of Gastrointestinal Pathophysiology, Institute of Natural Medicine, University of Toyama, Toyama, Japan.
authors.forename: Shusaku
authors.initials: S
authors.lastname: Hayashi
authors.affiliation: Division of Gastrointestinal Pathophysiology, Institute of Natural Medicine, University of Toyama, Toyama, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Kadowaki
authors.affiliation: Department of Obstetrics and Gynecology, University of Tokyo, Tokyo, Japan.
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Osuga
authors.affiliation: Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
authors.forename: Shigeru
authors.initials: S
authors.lastname: Saito
mesh_terms: D000157:Aconitine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000328:Adult; D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology / Q000276:immunology; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004195:Disease Models, Animal; D004715:Endometriosis / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D004717:Endometrium / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors / Q000494:pharmacology; D008262:Macrophage Activation / Q000187:drug effects; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D051379:Mice; D009538:Nicotine / Q000494:pharmacology; D061251:Primary Cell Culture; D011812:Quinuclidines / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D012333:RNA, Messenger / Q000819:agonists / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology*; D012720:Severity of Illness Index; D015398:Signal Transduction; D064569:alpha7 Nicotinic Acetylcholine Receptor / Q000819:agonists / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology*
chemical_list: D019086:Bridged Bicyclo Compounds, Heterocyclic; C508585:IL1B protein, human; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; C513163:N-(1-azabicyclo(2.2.2)oct-3-yl)furo(2,3-c)pyridine-5-carboxamide; D011812:Quinuclidines; D012333:RNA, Messenger; D064569:alpha7 Nicotinic Acetylcholine Receptor; C054634:methyllycaconitine; D009538:Nicotine; D000157:Aconitine
keywords: endometriosis; inflammation; nicotine; α-7 nAChR