| Project/Area Number |
12470324
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
ISSIKI Atsusi Tokyo Medical University Medicine Professor, 医学部, 教授 (60074796)
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| Co-Investigator(Kenkyū-buntansha) |
HAMADA Yoshikazu Tokyo Medical University Medicine Assistant Professor, 医学部, 講師 (50246279)
MIURA Hitoshi Tokyo Medical University Medicine Assistant Professor, 医学部, 講師 (50246302)
WATANABE Yasuo Tokyo Medical University Medicine Associate Professor, 医学部, 助教授 (70183720)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 2002: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2000: ¥6,700,000 (Direct Cost: ¥6,700,000)
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| Keywords | Brain cell environment / Neuronal cells / Glia / Cytokines / Neuroprotection / Chondroitinsulfuric acid / Extracellular matrix / サイトカイン療法 / 脳保護 / アシドーシス / 興奮性アミノ酸 / アポトーシス / 神経-グリア細胞 / 脳細胞環境系 / 静脈麻酔薬 / 脳保獲 / 培養脳神経細胞 / 培養脳グリア細胞 / Bcl-2 / Ca^<2+> / NOx |
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| Research Abstract |
Brain cell environment means the interaction between neuronal, glial and endotherial cells in the brain. In the brain cell environment, glia plays an important role for maintaining the brain functions. In our experiments which were performed by the Grant-in-Aid for Scientific Research (B), the neuronal cell cultures without glia were well-damaged and were induced a time-dependent NO production by the endotoxin and the acidosis because of less extracellular matrix (ECM) and less production of cytokines from glia. For instance, these stimulants induced much more contents of EL-8 and TNF a in the glia contained cells during the cell damages, although it is not cleared that these cytokines play as either pro- or anti-inflammatory factors. And the interaction between these cytokines under the brain cell damages might be different from that seen in the peripheral immune system. Additionally the cocultured neuronal cells with glia showed much stronger protection to the stimulants-induced brain cell death, when the pmol ranged chondroitinsulfuric acid derivative (CS-PE), one uf the extracellular modulators, was added to the cells. Our results indicate that the cytokine therapy to the brain dysfunction must be specifically established, since the cytokine network in the brain and peripheral immune system is dissimilar. Furthermore, CS-PE can be a potential treatment for the brain infarction.
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