Neuroprotective effect of AG490 in experimental traumatic brain injury of rats  

作　　者：DU Ai-ling JI Tai-ling YANG Bin CAO Jian-feng ZHANG Xing-guang LI Yu PAN Shun ZHANG Bo HU Zhen-bo ZENG Xian-wei 

机构地区：[1]Weifang Med Coll, Affiliated Hosp, Dept Neurosurg, Weifang 261031, Shandong, Peoples R China [2]Weifang Med Coll, Affiliated Hosp, Dept Stem Cell Transplantat, Weifang 261031, Shandong, Peoples R China [3]Weifang Med Coll, Affiliated Hosp, Res Ctr, Weifang 261031, Shandong, Peoples R China

出　　处：《Chinese Medical Journal》2013年第15期2934-2937,共4页中华医学杂志（英文版）

基　　金：This study was supported by grants from the Natural Science Foundation of Shandong Province，the Science and Technology Research Program of Shandong Province

摘　　要：Background Traumatic brain injury （TBI） is a major cause of death and disability in children and young adults worldwide. Therefore, we investigated the role of AG490 in regulating brain oedema, expression of CD40 and neurological function after TBI. Methods Sprague Dawley rats （n=240） were randomly divided into a sham operation group, TBl＋saline group and TBI＋AG490 （JAK/STAT inhibitor） group, Members of each group were euthanized at 6, 12, 24 or 72 hours after injury. Neurological severity score （NSS） was used to evaluate the severity of neurological damage. Brain water was quantitated by wet/dry weight method. The expression of CD40 was assessed by flow cytometry. Results In both the TBl＋saline group and the TBI＋AG490 group, the brain water content was elevated after TBI, reached a peak at 24-hour and remained high for the rest of the pedod investigated; the expression of CD40 reached a peak 24 hours after TBI; the NSS was elevated after TBI and then decreased after 6 hours. Elevations in the Level of CD40, degree of brain edema and NSS after TBI were significantly reduced in TBI＋AG490 group. Conclusion Inhibition of the JAK/STAT signalling pathway reduces brain oedema, decreases the expression of CD40 and exerts neuroprotective effects after TBI.Background Traumatic brain injury （TBI） is a major cause of death and disability in children and young adults worldwide. Therefore, we investigated the role of AG490 in regulating brain oedema, expression of CD40 and neurological function after TBI. Methods Sprague Dawley rats （n=240） were randomly divided into a sham operation group, TBl＋saline group and TBI＋AG490 （JAK/STAT inhibitor） group, Members of each group were euthanized at 6, 12, 24 or 72 hours after injury. Neurological severity score （NSS） was used to evaluate the severity of neurological damage. Brain water was quantitated by wet/dry weight method. The expression of CD40 was assessed by flow cytometry. Results In both the TBl＋saline group and the TBI＋AG490 group, the brain water content was elevated after TBI, reached a peak at 24-hour and remained high for the rest of the pedod investigated; the expression of CD40 reached a peak 24 hours after TBI; the NSS was elevated after TBI and then decreased after 6 hours. Elevations in the Level of CD40, degree of brain edema and NSS after TBI were significantly reduced in TBI＋AG490 group. Conclusion Inhibition of the JAK/STAT signalling pathway reduces brain oedema, decreases the expression of CD40 and exerts neuroprotective effects after TBI.

关 键 词：AG490 traumatic brain injury brain edema CD40 neurological severity score 

分 类 号：Q257[生物学—细胞生物学] F407.7[经济管理—产业经济]