| Project/Area Number |
15K10681
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Kitawaki Jo 京都府立医科大学, 医学(系)研究科(研究院), 教授 (00204925)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 子宮内膜症 / エストロゲン関連受容体 / GPER1 / アグリコン型イソフラボン |
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| Outline of Final Research Achievements |
Endometriosis is one of estrogen-dependent diseases. In endometriosis tissue, the expression level of estrogen receptor (ER)β is higher than that of ERα. Endometriosis also expresses estrogen-related receptor (ERR) α, β, γ, and a transmembrane receptor GPER1.
Using primary cultured cell line derived from endometriosis and mouse endometriosis model, we demonstrated that G1, a GPER1 agonist, induces apoptosis by non-genomic action. Furthermore, we demonstrated that AglyMAX, an aglycone-type isoflavone with weak estrogen action, suppresses proliferation of endometriotic cells and cystic lesion of mouse model via the ERβ-NFκB pathway. AglyMAX inhibits various inflammatory factors.
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