摘要
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 explore the regularity of the change of nitric oxide synthase(NOS) in hippocampus CA 1 area by incomplete cerebral ischemia and reperfusion in different period,and to investigate the effects of monosialoganglioside on the change of the number of NOS positive cells and the protection of neurons. Methods:The rat models of incomplete cerebral ischemia and reperfusion in different period were established by bilateral carotid artery clamping combined with blooding. NADPH diaphorase histochemistry was used to investigate the postischemia changes of NOS in CA 1 in the models and the effects of GM 1 on them were observed. Results:Neurons in CA 1 were damaged. The number of NOS positive cells in CA 1 (44.5±7.4) was maximal to about 2 times higher than the normal control group at 30 min following incomplete ischemia and was decreased gradually at 2 h,12 h,24 h,3 d after reperfusion and turned to normal level in 5d. GM 1 could inhibit their increase and protect the neurons in CA 1 from damage in ischemia and reperfusion in different period.Conclusion:GM 1 could inhibit the expression of NOS positive neurons in CA 1 following incomplete ischemia and reperfusion in different period and has protected effect on the neurons.
基金
国家教委基金资助项目 (教外司留 80 6号 )
