The molecular phamacological study of the interaction of neuro-immune system

炎症/免疫过程是脑缺血后神经细胞存活/损伤的基础。目前尚不清楚脑缺血后神经元死亡是凋亡还是坏死。在短暂性前脑缺血条件下，我们得到的结果表明，CA1区锥体神经元迟发性死亡与细胞凋亡有关。在胶质细胞中，在缺血应激后产生IL-1β、肿瘤坏死因子-α等细胞因子。另一方面，也提示NO/iNOS参与了神经细胞的凋亡。短暂性前脑缺血后，星形胶质细胞主要表达诱导型一氧化氮合酶(INOS)，同时观察到神经元的凋亡。在下一个系列中，我们检查了脑缺血后是否产生了细胞因子和趋化因子。观察短暂性前脑缺血后大脑皮层和海马区IL-6和CINC基因的瞬时表达。IL-6被认为是神经元的生存因子。因此，IL-6可能作为一种保护因子发挥抗缺血应激的作用。NO、细胞因子和趋化因子在脑缺血损伤中的确切作用是一个需要阐明的有趣课题。

Inflammatory/immnological processes underlie survival/damage of meurons after brain ischemia. It is not clear whether or not the neuronal death after brain ischemia is apoptosis or necrosis. Under the condition of transient forebrain ischemia, we obtained results suggesting apoptosis in the delayd neuronal death of the CA1 pyramidal neurons.In glia ; cells, cytokines such as IL-1beta asnd TNF-alpha are produced following ischemic stresses. On the other hand, it is suggested that NO/iNOS is involved in neuronal apoptosis. The iNOS induction was detected primarily in astrocytes after the transient forebrain ischemia when the neuronal apoptosis was observed. In the[next series, we examined whether cytokines and chemokines were produced after the brain ischemia. The transient expressions of mRNA of IL-6 and CINC were observed after the transient forebrain ischemia in the cerebral cortex and the hippocampus. IL-6 is known as a survival factor for neurons. It is, therefore, suggested that IL-6 may play a role as a protective factor against ischemic stress. The precise roles of NO,cytokines and chemokines on brain ischemic insult are an interesting subject to be elucidated.