Journal Title
Title of Journal: Cell Mol Neurobiol
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Abbravation: Cellular and Molecular Neurobiology
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Authors: Danying Su Jing Ma Zhuobo Zhang Ye Tian Baozhong Shen
Publish Date: 2015/10/01
Volume: 36, Issue: 6, Pages: 907-914
Abstract
This study was aimed to investigate the treatment mechanisms of 552nitrophenyl furfuryliodine13diphenyl2thiobarbituric acid UCF101 in cerebral ischemia–reperfusion CIR model rats Total of 54 healthy male Wistar rats were randomly assigned into three groups namely sham group vehicle group and UCF101 group The CIRinjured model was established by right middle cerebral artery occlusion and reperfusion Neurological function was assessed by an investigator according to the Longa neurologic deficit scores Meanwhile the cerebral tissue morphology and apoptotic neurons were evaluated by HE and TUNEL staining respectively Additionally the expressions of caspase 3 pp38 and pERK were detected by immunohistochemistry or/and Western blotting assays As results neurologic deficit and pathological damage were obviously enhanced and TUNEL positive neurons were significantly increased in CIRinjured rats as compared with those in sham group Furthermore the expressions of caspase 3 pp38 and pERK were also significantly increased in vehicle group than those in sham group P 005 However UCF101 treatment could markedly weaken the neurologic deficit with lower scores and improve pathological condition After UCF101 treatment TUNEL positive neurons as well as the expression of caspase 3 were significantly decreased than those in vehicle group P 005 Besides pp38 was decreased while pERK was increased in UCF101 group than those in vehicle group P 005 Therefore we concluded that the protective effects of UCF101 might be associated with apoptosis process and MAPK signaling pathway in the CIRinjured model
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