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目的 :研究一氧化氮 ( NO)在缺血性海马迟发性神经元死亡 ( DND)中的作用 ,观察非选择性一氧化氮合酶 ( nitricoxidesynthase,NOS)抑制剂 NG-nitro-L-arginine( L-NNA)对缺血性海马 DND的影响。方法 :实验分为假手术组、生理盐水治疗组、L-NNA治疗组。采用大鼠 4血管关闭方法制作了全脑缺血再灌流模型 ,以假手术组为对照 ,检测了脑缺血 1 0 min再灌流 72 h海马区 NOS活性的变化并观察计量了海马 CA1 区组织病理改变 ;同时观察了 L-NNA对海马区 NOS活性和 CA1 区病理改变的影响。结果 :生理盐水治疗组海马组织 NOS活性显著升高( P<0 .0 1 ) ,L-NNA可部分抑制海马区 NOS活性 ( P<0 .0 1 ) ,使海马 CA1 区神经元存活数显著增加 ( P<0 .0 1 )。结论 :NO在海马 CA1 区 DND发生中具有毒性作用 ,L-NNA对海马 CA1 区神经元损伤有一定的保护作用。
Objective: To investigate the role of nitric oxide (NO) in the delayed neuronal death (DND) in ischemic hippocampus and to observe the effects of non-selective nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine (L-NNA) on ischemic hippocampal DND. Methods: The experiment was divided into sham operation group, saline treatment group and L-NNA treatment group. The rat model of global cerebral ischemia-reperfusion was established by the rat 4-vessel occlusion method. The sham-operation group was used as a control. The changes of NOS activity in the hippocampus after reperfusion for 10 min were detected and the changes of hippocampal CA1 region Meanwhile, the effect of L-NNA on the activity of NOS and the pathological changes of CA1 in hippocampus were observed. Results: The activity of NOS in hippocampus of NS group was significantly increased (P <0.01). L-NNA partially inhibited the activity of NOS in hippocampus (P <0.01), and significantly increased the number of neurons in hippocampal CA1 area Increase (P <0. 01). CONCLUSION: NO has a toxic effect on DND in hippocampal CA1 region, and L-NNA may protect neurons in hippocampal CA1 region.