短暂陛全脑缺血/再灌注损伤致大鼠海马组织BNIP3表达水平的改变

目的 观察全脑缺血/再灌注损伤后大鼠海马组织Bc12/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)、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.western blot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72 h组中海马CAI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1 h组(2.543±0.473)与全脑缺血/再灌注6 h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1 h组与全脑缺血/再灌注6 h组间比较差异无统计学意义(P>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.

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

Objective To study the changes in Bcl-2/adenovirus EIB 19kD-interacting protein 3(BNIP3)expression in the hippocampus of rats following transient forebmin ischemia. Methods Ten adult male Wistar rats were randomized into sham operation group(n=5)andischemia-rcperfosion group(n=5),and the rats in the latter group were subjectedto global ischemia for 15 min followed by repeffusion for 72 h.Nissl's staining was used to examine the neuronal death in the hippocampus induced by global brain isehemia.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 isehemia followed by reperfusion for 1 h(n=5),and group 3 with global isebemia 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 hippoeampal Cal region,where the neurons presented with irregular shape,cell shrinkage and nuclear fragmentation. BNIP3 monomer expression significantly increased in the hippocampus after isehemia-reperfusion in comparison with that in the sham operation group(P<0.05),but the length of reperfusion time(1 and 6 h)did not significantly affected BNIP3 monomer expression (2.543±0.473vs3 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.