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作 者:韩冬[1] 孙淼[1] 何平平[1] 温璐璐[1] 张鸿[1] 冯娟[1]
机构地区:[1]中国医科大学附属盛京医院神经内科,辽宁沈阳110004
出 处:《中风与神经疾病杂志》2015年第4期296-298,共3页Journal of Apoplexy and Nervous Diseases
基 金:辽宁省博士启动基金项目(No.20121131);辽宁省科学计划重大;重点项目;重大疾病动物实验研究及临床应用项目编号(No.2012225021)
摘 要:目的观察缺血后处理对脑缺血再灌注后紧密连接的保护作用及相关蛋白ZO-1表达的影响。方法 45只Wistar雄性大鼠随机分为假手术(Sham)组、缺血再灌注(I/R)组、缺血后处理(IP)组。采用线栓法建立大鼠大脑中动脉缺血模型,脑缺血2 h后,I/R组予再灌注,IP组给予缺血后处理之后予再灌注。于脑缺血再灌注后24 h行TTC染色观察脑梗死体积,应用电镜观察紧密连接蛋白结构改变,Western blot观察ZO-1蛋白表达的变化。结果 IP组脑梗死体积明显小于I/R组,与Sham组相比,I/R组血脑屏障紧密连接开放,ZO-1蛋白表达明显减少;与I/R组比较,IP组紧密连接开放程度减轻及ZO-1表达增加。结论缺血后处理减小脑梗死体积;缺血后处理能够减轻紧密连接破坏,其保护机制可能与ZO-1蛋白表达增加有关。Objective To investigate the effects of ischemic postconditioning on tight junction and influence on expression of ZO-1 protein after ischemia / reperfusion. Methods 45 adult male Wistar rats were randomly divided into Sham group,ischemia / reperfusion( I / R) group,and ischemic postconditioning( IP) group. Models were induced by focal ischemia for 2 h with middle cerebral artery occlusion( MCAO) and 24 h reperfusion. Rats in IP group were treated with postconditioning after 120 min of occlusion. Twenty-four hours after reperfusion,the rats were killed and the brains were stained by 2,3,5-triphenyltetrazolium chloride( TTC) to measure the size of infarct. We used transmission electron microscopy to observe the structure of tight junction and used Western blot analysis to measure the expression of ZO-1 protein,and compared the differences among groups. Results In IP group,sizes of infarct were extremely smaller than that in I / R group.Compared with those in the Sham group,tight junctions were opened and the expression of ZO-1 was lower in I / R group.While in IP group,We observed that the structure of tight junction was better and more ZO-1 protein was expressed.Conclusion Ischemic postconditioning could decrease the size of infarcts. Ischemic postconditioning could protect tight junction from I / R injury. Its mechanism may be relation to the up-regulation expression of ZO-1 protein.
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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