Trearment for DIND and DND after subarachnoid hemorrhage

蛛网膜下腔出血(SAH)后，c-fos和c-jun基因在大脑皮层、海马区和海马齿状回均有表达。Hsp7O基因在受累侧大脑皮层、海马、丘脑、下丘脑和尾壳核均有表达，并延伸至对侧。在TUNEL法中，SAH后48h，只有穿通侧Cal神经元出现凋亡样改变。Bax和P53基因在CAL中有较强的诱导作用，高峰出现在12h~48h之间，可能是导致细胞凋亡的原因，而bcl2也在同一时期上调。P53对bax/bcl2比值的调节可能影响细胞的凋亡。我们研究了低温对暴露于SAH的脑组织的影响。轻度低温抑制了大脑皮层、丘脑和海马区hsp7O基因的表达。C-jun基因在大脑皮层、丘脑和CA1区的表达也随着低温的降低而降低。在未来，我们认为亚低温治疗可能是治疗SAH的方法之一。

We have detected c-fos and c-jun mRNA in cerebral cortex, hippocampus and dentate gyrus in the penetrated side after subarachnoid hemorrhage (SAH). mRNA coding for hsp7O was induced in the cerebral cortex, hippocampus, thalamus, hypothalamus, and caudoputamen in the penetrated side and extended to the contralateral side. In the TUNEL.method, only CAl neurons in the penetrated side showed apoptosis-like changes 48hr after SAH.The genes for bax and p53 were induced fairly in the CAl with peak between l2hr and 48hr which might cause apoptosis, although bcl-2 was also upregulated during the same period. The regulation of bax/bcl-2 ratio through p53 might influence apoptotic cell death. We investigated the effect of hypothermia on brain exposed to SAH.Mild hypothermia depressed hsp7O mRNA expression in the cortex, thalamus and hippocampus. The c-jun mRNA expression was also reduced with hypothermia in the cortex, thalamus and CA1. In the future, we indicated that hypothermia therapy might be one of the procedures to treat SAH.