New approach to investigate the mechanisms of Ischemic neuronal death and development for the establishment of new way of brain resuscutator

脑缺血以延迟性神经细胞死亡的形式导致严重的损伤。我们从免疫抑制剂环孢素A(CsA)和FK506的作用机制方面探讨了迟发性神经细胞死亡的机制。从我们的研究结果来看，钙调神经磷酸酶和免疫亲和素信号转导通路在神经保护中起着重要的作用，尤其是线粒体异构酶环磷酰胺D在调节线粒体通透性转换孔形成方面起着关键作用，这也是我们还需要进一步分析以探索更多的机制。这些结果为临床应用和开发治疗脑以及心脏和肝脏缺血性损伤的新药提供了线索。

Brain ischemia leads to severe damage in the form of delayed neuronal cell death. We have been investigated the mechanisms of delayed neuronal cell death in terms of the mechanisms of immunosuppressant, such a cyclosporin A(CsA) and FK506. From our results, Calcineurin and immunophilin signal transduction casca* play an important roles for neuroprotection, Especially, mitochondrial isomerase cyclophillinD paly a pivotal role to regulate the MPT(Mitochondrial Permeability Transition)pore formation, one of the prolylcis/trans isomerase family members.We also need further analysis to explore more mechanisms.These results shed light on the clinical application and development of new drugs for the treatment of ischemic damage in the brain as well as in the heart and liver.