Development of new drugs based on molecular mechanism for infectious corneal ulcer
| Project/Area Number |
23592572
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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 |
Ophthalmology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SONODA Koh-hei 山口大学, 大学院医学系研究科, 教授 (10294943)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 角膜潰瘍 / 感染 / ｺﾗｰｹﾞﾝ分解 / MMP / コラーゲン分解 / 角膜 / 潰瘍 / 角膜線維芽細胞 / 性ホルモン |
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| Research Abstract |
Collagen degradation of corneal stroma relates to the etiology of corneal ulcerration.Moreover,Corneal fibroblasts contribute to collagen remodeling in the corneal stroma in part by mediating collagen degradation.Corneal structure is influenced by sex hormone status,we examined the effects of sex hormones on collagen degradation by corneal fibroblasts.17beta-Estradiol and progesterone,female sex hormones,inhibited interleukin (IL)-1beta-induced collagen degradation,whereas testosterone and DHEA had no such effect.MMP expression and activation in corneal fibroblasts exposed to IL-1beta were also inhibited by them.They nhibited the IL-1beta-induced phosphorylation of p38 MAPK without affecting that of the MAPKs ERK or JNK.17beta-Estradiol also inhibited the IL-1beta-induced phosphorylation of IkappaB-alpha.Female sex hormones inhibited MMP expression and activity in IL-1beta-stimulated corneal fibroblasts and thereby suppressed collagen degradation by these cells.
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Report
(4 results)
Research Products
(30 results)
