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作 者:施建生[1] 高志伟[2] 秦建兵[2] 徐慧君[3] 包仕尧[1]
机构地区:[1]南通医学院附属医院神经内科,南通226001 [2]南通医学院神经生物研究所 [3]苏州大学医学院第二附属医院神经内科
出 处:《南通医学院学报》2004年第2期167-169,共3页ACTA Academiae Medicinae Nantong
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齿状回一氧化氮合酶(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 (NDAPH- d)组织化学方法观察缺血及再灌注后海马齿状回 NOS阳性神经细胞变化及 GM1 对其的影响。结果 :海马齿状回在缺血 30 min时 NOS阳性细胞数最高 (4 3.6 7± 6 .71) ,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。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齿状回Objective:To explore the regularity of the change of nitric oxide synthase(NOS) in hippocampus dentate gyrus 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 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. NDAPH-diaphorase histochemistry was used to investigate the postischemia changes of NOS in dentate gyrus in the model and the effects of GM 1 on them were observed.Results:The number of NOS-positive cells in dentate gyrus was maximal(43.67±6.71) at 30min following incomplete ischemia and was decreased gradually at 2h、12h、24h、3d after reperfusion and was at normal level in 5d(30.92±5.43). GM 1 could inhibit their increases in different period of the ischemia and reperfusion in dentate gyrus.Conclusion:GM 1 could inhibit the expression of NOS-positive neurons in dentate gyrus following incomplete ischemia and reperfusion in different period.
关 键 词:不完全性脑缺血 海马齿状回 一氧化氮合酶 神经节苷脂 大鼠
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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