急性缺氧小鼠海马CAl区NOS活力和nNOS蛋白表达的时程变化

Changes of NOS Activity and nNOS Expression in Hippocampal CAl of Mice during Acute Hypoxia

目的:观察急性缺氧小鼠海马CAl区一氧化氮合酶(NOS)和神经元型一氧化氮合酶(nNOS) 阳性神经元的时程变化,探讨NO在脑缺氧中的作用并为抗脑缺氧提供依据。方法:复制小鼠急性缺氧模型,采用NADPH-d组织化学和nNOS免疫组织化学方法,研究急性缺氧后不同时程点小鼠海马CAl区NADPH-d 和nNOS阳性神经元数量的变化。结果:与正常对照组相比较,急性缺氧后0.5h组小鼠海马CAl区NADPH-d 和nNOS阳性神经元的数量无明显变化,差异无显著性(P>0.05),3h、6h和12h组逐渐增多并于12h升高达到最高峰,差异有显著性(P<0.05),而于24h后开始降低,48h恢复正常。结论:急性缺氧后早期海马CAl区NOS和nNOS水平明显增多,NO在缺氧所致早期脑损伤中起重要作用。

Objective: To explore the vigor of nitric oxide synthase (NOS) and the expression level of neuronal nitric oxide synthase (nNOS) in the hippocampal CAl of mice during acute hypoxia. Methods: Model of acute hypoxic mice was duplicated, NADPH-d histochemistry and nNOS immunohistochemistry were used to investigate the changes of NOS in different groups. Results: Compared with the control group, the number of NADPH-d positive neurons and nNOS positive neurons in the hippocampal CAl didn't change in 0.5h group (P>0. 05), however, those were gradually increased in 3h group, 6h group, 12h group and it reached peak in 12h group(P<0. 05). In 24h group, those began to decrease and it recovered to baseline in 48h group. Conclusion: The increasing NOS might play an important role in brain damage during acute hypoxia.