| Project/Area Number |
17K01477
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
五十嵐 博中 新潟大学, 脳研究所, 教授 (20231128)
若林 あや子 日本医科大学, 医学部, 講師 (30328851)
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| Project Period (FY) |
2017-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | gut microbiota / ischemic stroke / mice / 腸内細菌 / 抗生物質 / 脳梗塞 / distal MCA / 脳梗塞モデル / 腸管上皮細胞 / マウス / 腸内細菌叢 / IEL |
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| Outline of Final Research Achievements |
Cerebral infarction causes complications in the nervous and digestive systems, and one of the mechanisms is thought to involve changes in the intestinal microbiota after cerebral infarction. During the period of this study, due to changes in the research environment caused by the new coronavirus infection, the setting up of a mouse model of cerebral infarction was interrupted, and even after it was resumed, problems such as a high mortality rate emerged, forcing a change in the model plan.
Under these circumstances, they used the cerebral infarction model developed by Professor Tomohiro Matsuyama of Hyogo Medical University, in which the MCAs of SCID and CB-17 mice were directly electrocoagulation and ligated. Although the plan has been changed, the experiment is still ongoing in collaboration with other researchers by collecting brain, intestinal tract, and blood samples from the infarction and sham groups and measuring various cytokines, HMGB1, etc.
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| Academic Significance and Societal Importance of the Research Achievements |
脳梗塞患者の半数以上が便秘、便失禁、消化管出血などを呈するが、そのメカニズムの詳細は不明である。脳卒中患者は4-5倍排便困難症に罹患しやすく、また、約30－60％と高頻度に起こることが知られているが、このメカニズムの一つとして脳卒中後の腸内細菌叢の変化が関与すると考えられている。我々は未だ検討途中であるものの、脳梗塞病変部位組織および盲腸組織のRNAシーケンシングにより脳梗塞部位の細胞死と炎症の特徴について調べる。また、血中に放出されるエクソソーム中のシーケンシングも行い、腸管機能に変化を及ぼす可能性のあるmiRNAを検討し、これらのメカニズムを解明していく。
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