| Project/Area Number |
25870456
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
Neurosurgery
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| Research Institution | Okayama University |
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Principal Investigator |
DEGUCHI Kentaro 岡山大学, 医歯(薬)学総合研究科, 講師 (80467753)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 慢性期脳梗塞 / 再生治療 / 血液脳関門 / 脳保護療法 / 神経再生医療 / ペリサイト / tPA / エダラボン / テルミサルタン / PPARγ |
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| Outline of Final Research Achievements |
Changes of pericytes in the neurovascular unit (NVU) after the cerebral ischemia in rats were examined in relation to the effects of exogenous tissue plasminogen activator (tPA) and a free radical scavenger, edaravone. Immunohistochemistry and Western blot analyses showed that the overlap between pericytes and endothelial cells increased significantly at 4 days after 90 min of transient middle cerebral artery occlusion (tMCAO). The number of pericytes and the overlap with endothelial cells decreased with tPA, but recovered with edaravone 4 days after tMCAO with proliferation. Thus, tPA treatment damaged pericytes resulting in the detachment from astrocytes and a decrease in GDNF secretion. However, treatment with edaravone greatly improved tPA-induced damage to pericytes. The present study demonstrates that exogenous tPA strongly damages pericytes and destroys the integrity of the NVU, but edaravone treatment can extremely ameliorate such damage after acute cerebral ischemia in rats.
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