摘要
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 observe the effects of NBP on the change of nitricoxide（NO） in hippocampus after chronic hypoperfusion.Methods Eighty healthy Wistar rats were randomly divided into four groups：sham operation,experimental group,preconditioning group and treatment group.According to nitrate reductase method and β-NADPH,every group was divided into two subgroups.In the experimental group,preconditioning group and treatment group,two common carotid arteries were blocked to establish models of cerebral ischemia,and in the sham-operated group,the common carotid arteries were not ligated.Preconditioning group was given NBP before and after operation.Treatment group was given NBP after operaton,sham operation and experimental group was given normal saline.All rats were killed at 30 days after model establishment respectively.By nitrate reductase method,the abnormal changes of the content of NO in hippocampus were studied after rat forebrain ischemia.Nitric oxide synthase（NOS） positive neurons were stained by β-NADPH and analyzed under microscope.Results In comparison with sham-operated group,the content of NO and the numbers of NOS positive neurons increased in hippocampus of the rats in the experimental group,preconditioning group and treatment group respectively.Compared with the experimental group,the content of NO and the numbers of NOS positive neurons decreased in hippocampus of the rats in preconditioning group and treatment group.Compared with treatment group,the content of NO and the numbers of NOS positive neurons decreased in hippocampus of the rats in preconditioning group.Conclusion The content of NO in hippocampus are increased by 2VO,and this change could be relieved by NBP.
出处
《中国实用神经疾病杂志》
2012年第5期5-8,共4页
Chinese Journal of Practical Nervous Diseases
基金
山东省潍坊市卫生局科技发展项目(2011019)
关键词
丁基苯酞
慢性脑缺血
海马
一氧化氮
一氧化氮合酶
Butyphthalide
Chronic hypoperfusion
Hippocampus
Nitricoxide
Nitric oxide synthase
