摘要
目的观察环孢素A(Cyclosporin,CSA)对大鼠脑缺血再灌注损伤后小胶质细胞(microglia,MG)活化及诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)表达的影响,探讨其脑保护作用的可能机制。方法将SD大鼠随机分为假手术组、模型组、环孢素A组。改良线栓法制备建立局灶性脑缺血-再灌注动物模型,即大脑中动脉闭塞(MCAO)模型,分别于手术后1d,3d,7d,14d免疫组化法观察大鼠海马一区OX-42及iNOS的表达情况,同时对大鼠神经行为学进行评分。结果模型组、环孢素组1d即有OX-42的大量表达,3d时OX-42达到高峰,14d时接近正常;iNOS 1d达峰,7d及14d时接近正常。环孢素组OX-42、iNOS较模型组减少(P<0.05),且神经行为学评分优于模型组(P<0.05)。结论小胶质细胞的激活及iNOS大量表达和脑缺血-再灌注损伤密切相关,环孢素A可显著减少脑缺血再灌注损伤后小胶质细胞的激活和iN-OS的表达,对大鼠脑缺血再灌注损伤有一定的保护作用。
Objective To observe the effect of cyclosporin A （cyclosporine, CSA） on activation of microglia and expres- sion of iNOS after cerebral ischemia reperfusion injury in rats, and to investigate the protective mechanism of the brain. Meth- ods Rats were randomly divided into the sham-operative group, model group and cyclosporine group. The focal cerebral ische- mia-reperfusion injury models were made by suture-occluded method, namely the middle cerebral artery occlusion （MCAO） model. The expressions of OX-42 and iNOS in the rats hippocampal CA1 was detected by immunohistochemistry staining at 1st, 3rd, 7th and 14th day after operation. The score of behavior obstacle in rats was rated at the same time. Results In the model group and cyclosporine group, the number of OX-42 positive cells markedly appeared at 1st clay of reperfusion, then peaked at 3rd day of reperfusion, and it decreased nearly normal at 14th day. iNOS peaked at 1st day, at 14th and 7th day it closed to normal. Compared with model group, the expressions of OX-42 and iNOS in cyclosporine group were reduced （P〈0.05）, and the cyclosporin A group got better score of behavior obstacle（P〈0.05）. Conclusion The activation of microglia and expression of iNOS are closely associated with cerebral ischemia-reperfusion-injury. Cyclosporine A could significantly reduce the activation of microglia and expression of iNOS after ischemia-reperfusion-injury, has protective effect on ischemiareperfusion-injury in rats.
出处
《中国实用神经疾病杂志》
2010年第24期8-11,共4页
Chinese Journal of Practical Nervous Diseases
