p38 MAPK-BCL-xL pathway was involved in HPC-induced neuroprotection in ischemic brain of mice
会议名称：《中国生理学会第23届全国会员代表大会暨生理学学术大会》
会议日期：2010年
学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学]
基 金：supported by the following grants:the National Natural Science Foundation of China(30871219) China 973 Program (2006CB504100) Key Scientific Developing Program of Beijing Municipal Commission of Education(KZ200810025012) Beijing Municipal Program for Hundred-Thousand-Ten Thousand Excellent Talents of New Century(Li J) Funding Project for Academic Human Resources Development in Institutions of Higher Learning under the Jurisdiction of Beijing Municipality(PHR200906116)
关 键 词：HPC MCAO apoptosis BCL-xL p38 MAPK
摘 要：正Objective:To explore the role of p38 mitogen actived protein kinase（p38 MAPK）-BCL-xL antiapoptotic pathway in hypoxic preconditioning（HPC）-induced neuroprotection in ischemic ***:Male BALB/c mice（18-22 g,8-10 weeks） were randomly divided into four groups:H0 sham（H0+S）,normoxic ischemia（H0+I）, HPC sham（H4+S） and HPC-ischemia（H4+I） *** HPC and middle cerebral artery occlusion（MCAO）- induced focal cerebral ischemia mouse models,and combined with TUNEL staining and Western blot techniques, changes in neural apoptosis in the penumbra of ischemic cortex,antiapoptotic protein BCL-xL distribution in cytosol or mitochondria and the affection of p38 MAPK inhibitor SB203580 were *** addition,the interaction between BCL-xL and p38 MAPK was determined by using immunoprecipitation ***:HPC could inhibit neural apoptosis and elevated BCL-xL protein level in mitochondria significantly（P0.05,n=6 per group） in the penumbra of ischemic *** injection of p38 MAPK inhibitor SB203580 abolished the HPC-induced ***,the result of immunoprecipitation showed that there was an interaction between BCL-xL and p38 ***:HPC could protect the brain against MCAO-induced ischemic injuries via d38 MAPK-BCL-xL antiapoptotic pathway in mice.