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大鼠脑缺血再灌注损伤后磷酸化JAK2、STAT3蛋白表达及细胞凋亡
引用本文:谢惠芳,徐如祥,魏继鹏,姜晓丹,刘振华.大鼠脑缺血再灌注损伤后磷酸化JAK2、STAT3蛋白表达及细胞凋亡[J].南方医科大学学报,2007,27(2):208-211,218.
作者姓名:谢惠芳  徐如祥  魏继鹏  姜晓丹  刘振华
作者单位:1. 南方医科大学珠江医院,神经内科,广东,广州,510282
2. 南方医科大学珠江医院,神经外科,广东,广州,510282
摘    要:目的 观察磷酸化JAK2、磷酸化STAT3蛋白在局灶性脑缺血再灌注损伤后的表达及细胞凋亡的变化.方法 采用大脑中动脉线栓法制作大鼠局灶性脑缺血再灌注损伤模型,应用免疫组织化学及Western blotting检测大鼠局灶性脑缺血再灌注损伤后磷酸化JAK2、磷酸化STAT3蛋白表达水平的变化.利用原位缺口末端标记法研究神经细胞凋亡的变化.结果 与假手术组大鼠相比,脑缺血再灌注损伤后磷酸化JAK2、磷酸化STAT3蛋白表达明显增强,以缺血周边区表达最明显,再灌注24 h达高峰,之后开始下降,再灌注168h仍有少量表达.缺血再灌注损伤后凋亡细胞也显著增多,再灌注24h达高峰,凋亡细胞的变化与磷酸化JAK2、磷酸化STAT3蛋白表达变化一致.结论 脑缺血再灌注损伤后引发JAK2、STAT3的活化及超量表达可能与神经细胞生存和凋亡有关,JAK2/STAT3信号通路可能参与了脑缺血再灌注损伤与修复的病理生理过程.

关 键 词:脑缺血再灌注  蛋白质酪氨酸激酶  信号转导和转录激活子  凋亡
文章编号:1673-4254(2007)02-0208-05
收稿时间:2006-05-21
修稿时间:2006年5月21日

P-JAK2 and P-STAT3 protein expression and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats
XIE Hui-fang,XU Ru-xiang,WEI Ji-peng,JIANG Xiao-dan,LIU Zhen-hua.P-JAK2 and P-STAT3 protein expression and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats[J].Journal of Southern Medical University,2007,27(2):208-211,218.
Authors:XIE Hui-fang  XU Ru-xiang  WEI Ji-peng  JIANG Xiao-dan  LIU Zhen-hua
Institution:Department of Neurology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. xhffhx@126.com
Abstract:Objective To investigate the changes in phosphorylated JAK2 and STAT3 protein expression of and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats. Methods A rat models of focal cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion using modified filament method. Immunohistochemistry and Western blot analysis were used to detect the expression of P-JAK2 and P-STAT3 proteins, and TUNEL assay was employed to examine the cell apoptosis. Results P-JAK2 and P-STAT3 protein expression increased significantly after cerebral ischemia-reperfusion injury in rats. The immunoreactivity was prominent in the peripheral of the ischemic region and reached the peak level at 24 h of reperfusion, followed by slight decrement. The apoptotic cells increased obviously after cerebral ischemia-reperfusion injury, also reaching the peak level at 24 h of reperfusion. Conclusions The expression of phosphorylated JAK2 and STAT3 may be involved in the ischemic cellular events including apoptosis, JAK2/STAT3 signaling pathway plays a role in the pathophysiological process of cerebral ischemia/reperfusion cell injury and repair.
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