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作 者:施建生[1] 秦建兵[2] 徐慧君[2] 包仕尧[3]
机构地区:[1]南通医学院附属医院神经内科,江苏226001 [2]南通医学院附属医院神经生物研究所,江苏226001 [3]苏州大学医学院第二附属医院神经内科
出 处:《中国交通医学杂志》2004年第1期4-6,共3页Chinese Medical JOurnal of Communications
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大脑皮层一氧化氮合酶 (NOS)的影响。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大脑皮层NOS阳性神经细胞变化及GM1 对其的影响。结果 :大脑皮层在缺血 3 0min时NOS阳性细胞数最高 ( 12 .83± 4.49) ,再灌注 2h、12h、2 4h、3d后逐渐下降 ,5天时恢复正常水平。而GM1 能防止脑缺血及再灌注后NOS阳性神经细胞变化。结论 :GM1Objective:To explore the regularity of the change of nitric oxide synthase(NOS) in cerebral cortex by incomplete cerebral ischemia and reperfusion in different period,and investigate the effects of Monosialoganglioside on the change of the number of NOS-positive cells. Methods:The rat model of incomplete cerebral ischemia and reperfusion in different period was established by bilateral carotid artery clamping combined with blooding. NADPH-diaphorase histochemistry was used to investigate the postischemia changes of NOS in cerebral cortex in the model and the effects of GM 1.Results:The number of NOS-positive cells in cerebral cortex was maximal(12.83±4.49) at 30min following incomplete ischemia and was decreased gradually at 2h?12h?24h?3d after reperfusion and was normal level in 5d(7.36±1.58). GM 1 could inhibit their up-regulation in different period of the ischemia and reperfusion in dentate gyrus. Conclusions:GM 1 could inhibit the expression of NOS-positive neurons in cerebral cortex following incomplete ischemia and reperfusion in different period.
关 键 词:神经节苷脂 不完全性脑缺血 大脑皮层 NOS 神经元 一氧化氮合酶 再灌注损伤
分 类 号:R743.31[医药卫生—神经病学与精神病学]
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