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

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. Key words: Transient forebmin ischemia reperfusion;  Bcl-2/adenovirus E 1B 19kD-intemcting protein 3;  Hippocampus