小鼠不完全脑缺血再灌期前脑损伤及热休克蛋白的表达

目的：研究小鼠不完全脑缺血再灌用损伤的特点及热休克蛋白（ＨＳＰ）７０的表达。方法：暂时阻断小鼠双侧颈总动脉，再灌后２４或４８小时取材作光镜、电镜、ＴＵＮＥＬ染色及ＨＳＯ７０免疫细胞化学观察。结果：再灌２４小时海马ＣＡ１区见大量大缩的锥体细胞，电镜下可见核染色质聚积于核膜边和线粒体肿胀或空泡化等改变。皮层ＩＬ－ＶＩ层、扣带回、齿状回、尾壳核、海马ＣＡ３等处也见程度不同的受损细胞，外侧侧核细胞明显减少

REPERFUSION DAMAGE AND HEAT SHOCK PROTEIN 70 EXPRESSION IN MOUSE FOREBRAIN AFTER INCOMPLETE CEREBRAL ISCHEMIA

To investigate the reperfusion neuronal damage and heat shock protein(HSP) 70 expression in incomplete cerebral ischemic mice, the microstructure of forebrain was observed by TUNEL assay as well as HSP70 immunohistological method 24 to 48 hours later after temporarily occluding animal's bilateral carotids. It was found that extensive neuronal shrinkage with irregularly condensed nuclear appeared in the pyramidal layers of hippocampal CAI region 24 hours later after ischemia. Both the condensed chromatin abutting the nuclear membrane and the ultrastructure alterations such as mitochonderial swelling could be seen in this area. There existed abnormal morphological features in the II~VI layers of the cerebral cortex, cinguli and dentatus gyms, candoputamen and hippocampal CA3 regions to varying extent, and the cellular density in lateralis habenularis was greatly decreased. At the same time a great number of TUNEL-positive cells were scattered in the cortexes and hippocampus. The positive HSP70--immunoactive cells were found in the above regions of forebrain, while strong positive immunostain lay in the pyramidal cells in hippocampal CA3 and II--VI layer of the cerebral cortex. These results indicate that both necrosis and apoptosis may relate to the reperfusive forebrain damage in mice, and the HSP70 expression also involve in the forebrain's responses to cerebral ischemia-reperfusion stress.