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

脑缺血导致神经元细胞延迟死亡的严重损害。我们从免疫抑制剂环孢素a （CsA）和FK506的作用机制方面研究了延迟性神经元细胞死亡的机制。从我们的研究结果来看，钙调磷酸酶和亲免疫蛋白信号转导casca*在神经保护中发挥重要作用，特别是线粒体异构酶亲环酶ind在调节线粒体通透性转化（MPT）孔形成中起关键作用，MPT是prolylysis /trans异构酶家族成员之一。我们还需要进一步分析以探索更多的机制。这些结果为治疗脑、心、肝缺血性损伤的新药的临床应用和开发提供了启示。

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.