短暂性全脑缺血／再灌注损伤致大鼠海马组织BNIP3表达水平的改变  

BNIP3 expression is increased in the hippocampus of rats following transient global brain ischemia

作　　者：行艳丽[1] 朱心红[1] 严华成[1] 王璞[1] 李树基[1] 揭艳玲[1] 高天明[1] 

机构地区：[1]南方医科大学神经生物学教研室,广州510515

出　　处：《中华神经医学杂志》2008年第9期891-893,898,共4页Chinese Journal of Neuromedicine

基　　金：国家自然科学基金（U0632007,30330240）;973项目（2006CB5040101）

摘　　要：目的观察全脑缺血／再灌注损伤后大鼠海马组织Bcl2／腺病毒E1819kD相互作用蛋白3（BNIP3）表达水平的改变。方法取10只成年雄性Wistar大鼠，采用随机数字表法分为假手术组和全脑缺血／再灌注72h组．每组5只．通过尼氏染色检测缺血模型是否引起海马神经元死亡。另取14只成年雄性Wistar大鼠采用随机数字表法分为假手术组（4只1、全脑缺血／再灌注1h组（5只）、全脑缺血／再灌注6h组（5只）。在全脑缺血／再灌注后，于对应时间点取三组大鼠海马组织制备蛋白样品，Westernblot检测各时间点BNIP3表达水平的改变。结果（1）与假手术组比较，全脑缺血／再灌注72h组中海马CA1区神经元形态不规则，细胞皱缩，胞核碎裂消失，表明海马神经元死亡。（2）大鼠海马组织BNIP3单体表达水平在全脑缺血／再灌注后上调，与假手术组相比，全脑缺血／再灌注1h组（2．543±0．473）与全脑缺血／再灌注6h组（2．942±0．777）的海马组织BNIP3单体蛋白表达水平都升高，差异有统计学意义（P〈0．05），但全脑缺血／再灌注1h组与全脑缺血／再灌注6h组间比较差异无统计学意义伊〉0．05）。BNIP3双聚体在各时间点表达水平差异无统计学意义（P〉0．05）。结论全脑缺血／再灌注损伤可以引起大鼠海马组织BNIP3单体表达水平上调。Objective To study the changes in Bcl-2/adenovirus E 1B19kD-interacting protein 3 （BNIP3） expression in the hippoeampus of rats following transient forebrain ischemia. Methods Ten adult male Wistar rats were randomized into sham operation group （n=5） and ischemia-reperfusion group （n=5）, and the rats in the latter group were subjected to global ischemia for 15 min followed by reperfusion for 72 h. Nissl＇s staining was used to examine the neuronal death in the hippocampus induced by global brain ischemia. Another 14 adult male Wistar rats were randomly divided into 3 groups, namely group 1 with sham operation （n=4）, group 2 with global cerebral ischemia followed by reperfusion for 1 h （n=5）, and group 3 with global ischemia and reperfusion for 6 h （n=5）. All the rats were sacrificed to examine BNIP3 expression in the hippocampus using Western blotting. Results Compared with the sham operation group, the ischemia-reperfusion （72 h） group showed obvious neuronal death in the hippocampal CA1 region, where the neurons presented with irregular shape, cell shrinkage and nuclear fragmentation. BNIP3 monomer expression significantly increased in the hippocampus after ischemia-reperfusion in comparison with that in the sham operation group （P〈0.05）, but the length ofreperfusion time （1 and 6 h） did not significantly affected BNIP3 monomer expression （2.543±0.473 vs 2.942±0.777, P〉0.05）. No significant difference was found in the expression level of BNIP3 dimers between the sham operation, ischemia-reperfusion 1 h and 6 h groups （P〉0.05）.Conclusion The expression of BNIP3 is up-regulated in the hippocampus of rats with transient forebrain ischemia.

关 键 词：全脑缺血/再灌注 Bcl2/腺病毒E1819kD相互作用蛋白3 海马 

分 类 号：R743.31[医药卫生—神经病学与精神病学]