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目的 :探讨神经节苷脂 (GM1)对不完全性脑缺血及再灌注不同时间后海马CA1区一氧化氮合酶 (NOS)的影响及对神经元的保护作用。方法 :用双侧颈总动脉夹闭加放血的方法制成大鼠不完性脑缺血及再灌注模型 ,以还原尼克酰胺腺嘌呤二核苷酸脱氢酶 (NADPH d)组织化学方法观察缺血及再灌注后海马CA1区NOS阳性神经细胞变化及GM1对其影响。结果 :海马CA1区神经细胞受损 ,在缺血 30min时NOS阳性细胞数最高 (44 .5±7.4 ) ,为对照组的 2倍 ,再灌注 2h ,12h ,2 4h ,3d后逐渐下降 ,5d时恢复正常水平。而GM1能防止脑缺血及再灌注后神经细胞受损和NOS阳性神经细胞变化。 结论 :GM1对大鼠不完全性脑缺血及再灌注不同时间后海马CA1区NOS的表达有抑制作用 ,并对神经元具有保护作用。
Objective: To investigate the effect of ganglioside (GM1) on nitric oxide synthase (NOS) in the hippocampal CA1 area and its protective effect on neurons after incomplete cerebral ischemia and reperfusion. Methods: The model of incomplete cerebral ischemia and reperfusion in rats was made by bilateral common carotid artery occlusion plus blood perfusion, and the histochemical method of reducing nicotinamide adenine dinucleotide dehydrogenase (NADPH d) was observed Changes of NOS positive neurons in hippocampal CA1 subfields after ischemia and reperfusion and the effect of GM1 on them. Results: The number of NOS positive cells in the hippocampal CA1 region was impaired at 30min after ischemia (44.5 ± 7.4), which was twice as that in the control group and decreased gradually after 2h, 12h, 24h, When the return to normal levels. However, GM1 could prevent neuronal damage and NOS positive neurons after cerebral ischemia and reperfusion. CONCLUSION: GM1 can inhibit the expression of NOS in hippocampal CA1 subregion after cerebral ischemia and reperfusion in rats at different time points, and has a protective effect on neurons.