2015 Fiscal Year Final Research Report
PACAP38 suppresses cortical damage in mice with traumatic brain injury by enhancing antioxidant activity.
| Project/Area Number |
24791954
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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 |
Emergency medicine
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
OHTAKI hirokazu 昭和大学, 医学部 顕微解剖学, 講師 (20349062)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Keywords | 頭部外傷 / PACAP38 / 活性酸素種 / 酸化ストレス / 二次性損傷 / 神経保護作用 / 抗酸化酵素 |
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| Outline of Final Research Achievements |
The production of reactive oxygen species (ROS) and the resulting oxidative stress in mice in response to a controlled cortical impact (CCI) are typical exacerbating factors associated with traumatic brain injury (TBI).The aim of the present study was to determine whether PACAP38 exerts neuroprotective effects by regulating oxidative stress in mice with TBI. PACAP38 was administered intravenously immediately following CCI, and immunostaining for the oxidative stress indicator nitrotyrosine, and for neuronal death were measured 24 hours later. Western blot experiments to determine antioxidant activity in the neocortical region were also performed three hours post-CCI. . PACAP38 suppressed the extent of TBI and NT-positive regions 24 hours after CCI, and increased antioxidant enzymes in both hemispheres. Taken together, these results suggest that increasing antioxidant might activity isbe involving in one of the neuroprotective effect of PACAP38 in mice subjected to a CCI.
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| Free Research Field |
頭部外傷
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