慢性间断性缺氧诱导一氧化氮合酶表达的研究

目的:建立大鼠缺氧模型,检测神经元型一氧化氮合酶(nNOS)及诱导型一氧化氮合酶(iNOS)的表达情况。方法:1.建立缺氧模型:将SD大鼠置于常压低氧舱中,充入氮气调节氧浓度至所需氧浓度。2.动物分组:(1)急性缺氧组:在低氧舱中缺氧1.5小时。(2)慢性间断性缺氧组:每日在低氧舱中6小时。每周缺氧6天,共缺氧28天。3.采用免疫组化法检测nNOS和iNOS的表达。4.统计学分析检验。结果:急性缺氧后,iNOS、nNOS阳性神经元增加;慢性缺氧后,iNOS、nNOS阳性神经元仍持续增多,慢性缺氧时增加iNOS-IR细胞远远多于nNOS-IR细胞。结论:我们的研究表明缺氧可引起iNOS、nNOS阳性神经元增加,NOS亚型表达时间的不同说明其脑损伤具有阶段性。

Expression of nitric oxide synthase in rat brain during hypoxia

Objective: To establish an animal model of acute and chronic cerebral hypoxia in the rats, evaluate the expression of inducible nitric oxide(iNOS)and neuronal nitric oxide synthase(nNOS) and explore the possible mechanism of hypoxic brain injury. Methods: After the hypoxic models were made, The severity of hypoxic damage was assessed in the cortex and hippocampus by light microscopy. Immunocytochemistry was performed to detect the expression of iNOS and nNOS. The data were analyzed statistically. Results: iNOS-IR neurons appeared at 4th hour and reached peak at 5th hour after 1. 5 hours of hypoxia. Changes of nNOS-IR were not seen until 3rd day after hypoxia. Both iNOS-IR and nNOS-IR increased after 4 weeks of hypoxia. Conclusions: The results indicated that hypoxia which caused brain injury could induce the expression of nitric oxide synthases. NO might play an import role in brain damage during hypoxia.