New approach to investigate the mechanisms of Ischemic neuronal death and establishment of new way of brain resuscutation

低氧脑缺血导致严重的损伤，与前脑缺血延迟性神经元细胞死亡的形式类似。我们从免疫抑制剂环孢素A（cyclosporin A, CsA）和FK506的作用机制方面探讨了缺氧缺血性脑损伤的机制。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级联在神经保护中起重要作用。从我们的研究结果来看，钙调磷酸酶还调节Ca^<2+>稳态、HIF（缺氧诱导因子）和NCX（Na^+/Ca^<2+>交换器）。尤其是线粒体异构酶亲环酶（cyclophillinD）在调节线粒体通透性转化（MPT）孔形成中起着关键作用，它是脯氨酸顺/反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、肝缺氧缺血性损伤的临床应用和新药的开发提供了新的思路。

Hypoxic brain ischemia leads to severe damage as a similar form of delayed neuronal cell death in fore brain ischemia. We have been investigated the mechanisms of hypoxic ischemic brain damage in terms of the mechanisms of immunosuppressant, such as cyclosporin A(CsA) and FK506. From our results, Calcineurin and immunophilin signal transduction cascade play an important roles for neuroprotection. From our results, Calcineurin also regulates Ca^<2+> homeostasis, HIF(hypoxic inducible factor) and NCX(Na^+/Ca^<2+> exchanger). Calcineurin Especially, mitochondrial isomerase cyclophillinD paly a pivotal role to regulate the MPT(Mitochondrial Permeability Transition)pore formation, one of the prolyl cis/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 hypoxic ischemic damage in the brain as well as in the heart and liver.