| Project/Area Number |
26462490
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Tottori University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
原田 省 鳥取大学, 医学部, 教授 (40218649)
伊澤 正郎 鳥取大学, 医学部, 特任教授 (50032222)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 子宮内膜症 / 炎症 / マウスモデル / モデルマウス |
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| Outline of Final Research Achievements |
Local and chronic inflammatory reaction in the peritoneal environment is considered the contributing factors in the pathogenesis of the infertile patients with endometriosis. The inflammatory mediators, such as bacterial endotoxin, LPS (lipopolysaccharide), in the menstrual or peritoneal fluid, can activate the innate immune cells. A mouse endometriosis model was established by transplanting autologous endometrial tissue. LPS increased total number, size, and mRNA expression of the inflammation-related factors in murine endometriosis-like lesions, as human endometriotic tissues in the early stage.Treatment with a NFkB inhibitor negated these LPS-induced effects. LPS-induced pelvic inflammation status enhanced the development of murine endometriosis-like lesions via NFkB pathway.These data can be a molecular basis with regard to the strategy of novel treatment for the infertile patients with endometriosis.
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