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目的研究丁基苯肽对慢性脑缺血大鼠海马区一氧化氮(NO)表达的影响。方法 80只大鼠随机分为假手术组、模型组、预处理组、处理组。根据硝酸还原酶法和β-NADPH组织化学染色法,又将每个小组分为两个亚组。模型组、预处理组和处理组利用双侧颈总动脉永久结扎术制备动物模型,假手术组不结扎双侧颈总动脉。预处理组在造模前及造模后均给予丁基苯酞,处理组在造模后给予丁基苯酞,假手术组和模型组在造模后给予同等剂量的生理盐水,4组分别在造模后1个月处死大鼠取材。用硝酸还原酶特异性还原NO产物的方法测定大鼠前脑缺血模型中海马NO释放量的异常变化。β-NAD-PH组织化学染色显示一氧化氮合酶(NOS)阳性神经元,光镜下观察。结果模型组、预处理组及处理组海马区NO、NOS阳性神经元数目与假手术组相比均有明显增加。与模型组相比,预处理组和处理组海马区NO、NOS阳性神经元数目减少。与处理组相比,预处理组海马区NO、NOS阳性神经元数目减少更明显。结论慢性脑缺血缺氧能使大鼠海马区NO含量明显增加,丁基苯肽(NBP)能减轻这种变化。
Objective To investigate the effect of butylphthalide on the expression of nitric oxide (NO) in the hippocampus of rats with chronic cerebral ischemia. Methods 80 rats were randomly divided into sham operation group, model group, pretreatment group and treatment group. According to the nitrate reductase method and β-NADPH histochemical staining, each subgroup was divided into two subgroups. Animals in model group, pretreatment group and treatment group were perfused permanently with bilateral common carotid arteries. Bilateral common carotid arteries were not ligated in sham operation group. The pretreatment group was given butylphthalide before modeling and after modeling. Butylphthalide was given to the treatment group after modeling, and the sham operation group and model group were given the same dose of saline after modeling. Four groups Rats were sacrificed 1 month after modeling. The abnormal changes of NO release in the hippocampus of the rat forebrain ischemia model were determined by the specific reduction of NO by nitrate reductase. β-NAD-PH histochemical staining showed nitric oxide synthase (NOS) positive neurons, observed under light microscope. Results The numbers of NO and NOS positive neurons in hippocampus of model group, pretreatment group and treatment group were significantly increased compared with those in sham operation group. Compared with the model group, the number of NO and NOS positive neurons in the hippocampus of the pretreatment group and the treatment group decreased. Compared with the treatment group, the number of NO and NOS positive neurons in hippocampus of pretreatment group decreased more obviously. Conclusion Chronic cerebral ischemia and hypoxia can significantly increase NO content in hippocampus of rats, but butyl peptidyl peptide (NBP) can reduce this change.