| Project/Area Number |
18K16970
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56060:Ophthalmology-related
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 神経保護 / メラトニン / 緑内障 / アポトーシス / メラトニンレセプター / 網膜神経節細胞 / 神経保護療法 |
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| Outline of Final Research Achievements |
Although lowering of intraocular pressure is the only treatment for glaucoma, there are cases in which visual field impairment progresses even with sufficient lowering of intraocular pressure. It has been reported that it acts on cell death suppression and neuroprotection via melatonin receptors in the central nervous system.
This study was examined the possibility of neuroprotection by melatonin receptor regulation using NTG model rat. Compared with the control, the number of surviving retinal ganglion cells tended to be slightly higher with the administration of the melatonin receptor agonist and slightly lower with the administration of the melatonin receptor antagonist, but no significant difference was found between 3 groups. Bcl-2 was increased in the early stage by agonist administration, suggesting that melatonin receptor stimulation may increase anti-apoptotic factors and lead to survival of retinal ganglion cells.
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| Academic Significance and Societal Importance of the Research Achievements |
緑内障は本邦の中途失明原因の第1位を占める疾患であり、エビデンスのある唯一の治療方法は眼圧下降治療である。しかし、十分な眼圧下降でも視機能障害を抑制できないケースもみられ、眼圧以外の病態が関与している可能性が示唆されている。中枢神経におけるメラトニンレセプターを介した神経保護や内因性神経再生に関する報告が近年みられ、本研究では緑内障モデルを用いてメラトニンレセプターに着目した研究を行った。メラトニンレセプター制御により網膜神経節細胞死を抑制すると断定するには不十分な結果となったが、今後さらに検討を進めることでメラトニンレセプターと緑内障の関連性に関する新たな知見が得られるものと思われる。
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