诱导型一氧化氮合酶和缺氧缺血脑损伤

Inducible nitric oxide synthase and brain hypoxic-ischemic brain damage

摘要:

缺氧缺血可导致严重的神经系统疾病，如脑卒中、新生儿缺氧缺血性脑病。诱导型一氧化氮合酶在缺氧、缺血过程中被诱导表达，产生过量一氧化氮，导致神经系统的炎症反应及神经元死亡，加重神经损伤。抑制诱导型一氧化氮合酶表达在体内体外实验及临床应用中显示了一定的神经保护作用。该文综述了诱导型一氧化氮合酶在中枢神经系统中的表达及与缺氧缺血脑损伤的相关性，展望了诱导型一氧化氮合酶抑制剂作为缺氧缺血脑损伤治疗策略的前景。

Abstract:

Brain hypoxia-ischemia has been considered as critical factors in many human central nervous system diseases, including stroke and neonatal hypoxic-ischemic encephalopathy. In brain hypoxia-ischemia processes, inducible NO synthase（iNOS) is induced to produce excessive nitric oxide（NO) which leads to cascade reactions of inflammation and neuronal death, deteriorating primary brain injury. Inhibiting iNOS expression has opened new perspectives in the treatment of brain hypoxia-ischemia because iNOS inhibitor has been shown as a potent therapeutic agent. This reviews focus on recent research achievements regarding the relationship between iNOS and ischemic-hypoxic brain damage and the perspective of using iNOS inhibitors as therapeutic strategies for brain ischemic-hypoxic brain damage.