| Project/Area Number |
13671009
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Hiroshima International University Faculty of Health and Welfare (2002-2003)
Hiroshima University (2001) |
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Principal Investigator |
KAGAYA Ariyuki Hiroshima International University, Faculty of Health and Welfare, Professor, 医療福祉学部, 教授 (60274065)
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| Co-Investigator(Kenkyū-buntansha) |
MORINOBU Shigeru Hiroshima University, Graduate School of Biomedical Sciences, Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (30191042)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | neurosteroids / estradiol / cell damage / sodium fluoride / Neuro2A / thapshigargin / BAPTA / 細胞内カルシウム / beta-エストラジオール / デヒドロエピアンドロステロン / デヒドロエピアンドロステロン硫酸エステル / P450-SCC / 3-beta-HSD |
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| Research Abstract |
We examined the effect of various substances including neurosteroids on neuronal cell death using Neuro2A cultured cells, and found following results.
(1)Sodium fluoride (NaF) increased cell damage in a dose and time dependent manner with an EC5O value of 1mM on 24 hr exposure.
(2)Thapshigargin, Ca-ATPase inhibitor with an effect to increase cytosolic calcium, inhibited the cell damage induced by NaF, although thapshigargin itself produced small amount of cell death. These results suggest that NaF-facilitated cell damage is at least in part via a calcium-dependent mechanisms.
(3)As for neurosteroids, estradiol (10 and 30 micromolar) inhibited 3 mM NaF-induced cell death in a dose dependent manner. However, dehydroepiandrosterone or dehydroepiandrosterone sulfate, other neurosteroids, did not antagonized NaF-produced cell death.
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