摘要
目的 :探讨人参总皂甙 ( GS)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 ,以还原烟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阳性神经元变化及 GS对其的影响。结果 :单纯缺血组海马 CA1 区在缺血 30 m in时 NOS阳性细胞数最高 ( 4 4.5± 7.4 2 ) ,为假手术组 2倍 ,再灌注 2 h、12 h、2 4 h、3d后逐渐下降 ,5 d时恢复正常水平 ( 2 1.12± 3.5 0 ) ,缺血再灌注 3d、5 d时出现神经细胞损伤。GS能抑制缺血 30 min及再灌注各时程中 NOS阳性神经元数量变化 ,并能预防缺血再灌注后迟发的神经元损害。结论 :GS对大鼠不完全性脑缺血及再灌注不同时程后海马 CA1 区 NOS的异常表达有抑制作用 。
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 investigate the effects of total saponins of panax ginseng on the change of the number of NOS-positive cells and the protection of neurons. Methods:The rat model 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 model and the effects of GS on them was observed. Results:The number of NOS-positive cells in CA 1(44.5±7.42) was maximal to about 2 times higher than the normal control group at 30min following incomplete ischemia and was decreased gradually at 2h?12h?24h?3d after reperfusion and was at normal level in 5d(21.12±3.50). Neurons in CA 1 were damaged at 3d?5d after reperfusion. GS could inhibit their increases in ischemia and reperfusion in different period and protect the neurons in CA 1 from delayed damage after ischemia and reperfusion. Conclusion:GS could inhibit the expression of NOS-positive neurons in CA 1 following incomplete ischemia and reperfusion in different period and has protective effect on the neurons.
出处
《南通医学院学报》
2003年第1期12-15,共4页
ACTA Academiae Medicinae Nantong
关键词
不完全性脑缺血
海马CA1
一氧化氮合酶
人参总皂甙
大鼠
Incomplete cerebral ischemia
Hippocampus CA 1
Nitric oxide synthase
Total saponins of panax ginseng
Rat