脑缺血/再灌注前后一氧化氮合酶在脑皮质中的表达  被引量:2

The expression of NOS in the cortex before and after cerebral ischemia/reperfusion

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作  者:李健[1] 党辉[1] 沙晶[1] 艾山江[1] 景燕[1] 阿斯亚[1] 陆明佳[1] 补娟[1] 朱沂[1] 

机构地区:[1]新疆医科大学32期科研4-4班,乌鲁木齐830001

出  处:《疑难病杂志》2012年第4期280-282,F0003,共4页Chinese Journal of Difficult and Complicated Cases

基  金:新疆维吾尔自治区自然科学基金项目(No.2010211A56)

摘  要:目的观察小鼠脑缺血/再灌注(CIR)前后一氧化氮合酶(NOS)的3个亚型:神经元型(nNOS)、诱导型(iNOS)和内皮型(eNOS)在小鼠脑皮质中的变化,探讨NOS在CIR损伤后的不同作用。方法健康雄性ICR小鼠32只,随机分为假手术组(n=16)和短暂性大脑中动脉闭塞再灌注(tMCAO)模型组(n=16)。tMCAO模型组采用改良的线栓法制作,再灌注24 h后应用氯化三苯四氮唑(TTC)染色测量梗死体积,应用免疫组织化学法观察各组小鼠脑皮质中nNOS、iNOS和eNOS的表达。结果假手术组nNOS、iNOS和eNOS在脑皮质中少量表达,与假手术组比较,tMCAO组小鼠脑梗死体积明显增加;脑皮质区nNOS、iNOS和eNOS阳性细胞数均显著增多(P<0.05)。结论小鼠CIR损伤后,nNOS和iNOS表达的增加可以引起神经损伤,而eNOS表达的增加,可能发挥神经保护作用。Objective To investigate the changes of nNOS,iNOS and eNOS in the cortex before and after cerebral ischemia /reperfusion(CIR),to explore the roles of the subtypes of the NOS in CIR injury.Methods Thirty-two male ICR mice were divided into sham group(n = 16) and transient middle cerebral artery occlusion(tMCAO) model group(n = 16). The tMCAO group was induced with modified suture method and after 24 hours of reperfusion,and the infarct volume of the tMCAO group was measure with triphenyl tetrazo lium chloride(TTC).The expression of the nNOS,iNOS and eNOS in the cortex was observed 24 hours after the model building with immunohistochemistry.Results In sham group,the nNOS,iNOS and eNOS expressed a small amount in the cortex.After 24 hours of model building,the tMCAO group apparent stroke,the number of the positive cell of nNOS,iNOS and eNOS were all increased in the cortex in tMAO group(P 0.05).Conclusion After the CIR,the increased expression of nNOS and iNOS could cause nerve damage,and increased expression of eNOS may be play the role of neuro-protective.

关 键 词:脑缺血/再灌注 脑皮质 一氧化氮合酶 小鼠 

分 类 号:R743[医药卫生—神经病学与精神病学]

 

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