Objective To investigate the phosphorylation of Bad in cortex region of rats brain after ischemic preconditioning. Methods Four -vessel occlusion models (4 - VO)of Sprague - Dawley ( SD) rats were divided into three groups randomly: sham, cerebral ischemia - reperfusion ( I - R) and cerebral ischemic preconditioning ( CIP). The phosphorylation levels of Bad in cortex region were detected by immunohistochemistry. Results After the 3 d treatment in I - R group, p - Bad phosphorylation levels were gradually increased compared with the sham group ( P < 0. 05 ). At 3 d of reperfusion after CIP,p - Bad immunoreactivity increased markedly compared with ischemia - reperfusion group. Conclusion Our results indicate that the increasing activation of p - Bad might be one of the important factors induced cerebral ischemic tolerance mechanism.%目的 观察大鼠脑缺血预处理后皮质区Bcl-xl/Bcl-2相关死亡促进因子(Bcl-xl/Bcl-2 associated death promoter,Bad)磷酸化的表达及意义.方法 采用Sprague Dawley(SD)大鼠四动脉结扎全脑缺血模型,随机分为假手术组、缺血-再灌注组及缺血预处理组,免疫组织化学方法 检测各组大鼠脑内皮质区Bcl-xl/Bcl-2相关死亡促进因子磷酸化(p-Bad)的表达变化.结果 大鼠脑缺血-再灌注3 d后,缺血-再灌注组皮质区p-Bad表达逐渐增加,与假手术组比较差异有统计学意义(P<0.05),而缺血预处理组再灌注3 d p-Bad表达较缺血-再灌注组再灌注3 d显著增加(P<0.05).结论 缺血预处理对再次脑缺血有保护作用.
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