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

被引：19

作者：

Yamada-Nomoto, Kaori ^{[1
]}

Yoshino, Osamu ^{[1
]}

Akiyama, Ikumi ^{[2
]}

Ushijima, Akemi ^{[1
]}

Ono, Yosuke ^{[1
]}

Shima, Tomoko ^{[1
]}

Nakashima, Akitoshi ^{[1
]}

Hayashi, Shusaku ^{[3
]}

Kadowaki, Makoto ^{[3
]}

Osuga, Yutaka ^{[2
]}

Saito, Shigeru ^{[1
]}

机构：

[1] Toyama Univ, Dept Obstet & Gynecol, Toyama, Japan

[2] Univ Tokyo, Dept Obstet & Gynecol, Tokyo, Japan

[3] Toyama Univ, Inst Nat Med, Div Gastrointestinal Pathophysiol, Toyama, Japan

来源：

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY | 2016年 / 76卷 / 06期

关键词：

endometriosis; inflammation; nicotine; -7; nAChR; PROTEIN-KINASE INHIBITOR; COGNITIVE DEFICITS; IL-8; SECRETION; STROMAL CELLS; MURINE MODEL; SUPPRESSES; SMOKING; MICE; PROLIFERATION; EPIDEMIOLOGY;

D O I：

10.1111/aji.12592

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：491 / 498

页数：8

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