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作 者:杨小玉[1] 朱庆三[1] 赵立君[2] 孙庆[1] 秦彦国 段德生[1]
机构地区:[1]吉林大学中日联谊医院骨科,吉林省长春市仙台大街2号130031 [2]吉林大学体育学院运动医学系
出 处:《中国脊柱脊髓杂志》2004年第3期167-170,共4页Chinese Journal of Spine and Spinal Cord
基 金:吉林省自然科学基金项目(990563-1)
摘 要:目的:探讨脊髓缺血-再灌注损伤细胞间粘附分子-1(ICAM-1)及白细胞介素-1β(IL-1)的表达对血脊髓屏障损害的分子机制。方法:将77只同龄Wistar大鼠,随机分为正常对照组、单纯缺血组和缺血再灌组。手术方法采用Zivin法复制模型。应用逆转录-聚合酶链反应、地高辛标记cDNA探针技术、免疫组化及免疫荧光激光共聚焦扫描显微镜技术检测脊髓再灌注损伤血管内皮ICAM-1mRNA和IL-1βmRNA表达量。结果:正常组和单纯缺血组未引起细胞因子和粘附分子表达量的增加。而缺血再灌注后缺血区细胞因子、粘附分子的表达及多形核白细胞(PMN)的浸润先后发生了改变。再灌注2h,IL-1βmRNA的表达首先升高,约为对照组的2倍。再灌注6h达到高峰,并持续到12h。ICAM-1mRNA表达量于再灌注4h明显升高,再灌注12h其在单位微血管面积上的荧光强度约比单纯缺血组增加了1/2。结论:再灌注损伤后脊髓微血管内皮ICAM-1及其调节因子IL-1β的表达量增加是导致血脊髓屏障损害的重要分子基础。Objective:To investigate the molecular mechanism of expression of mircrovascular ICAM-1and its regulating factor IL-1βon damage of blood spinal cord barrier after spinal cord ischemia/reperfusion injury.Method:To set up spinal cord ischemia/reperfusion model.77Wistar rats were divided into control,ischemia and ischemia/reperfusion groups.The expression of vascular endotheliocytes ICAM-1mRNA and IL-1βmRNA in spinal cord injury was detected through the adoption of PCR,Digoxigenin marked cDNA probe technique,immunohistochemistry and immunofluorescence techniques.Result:The expression of cytokines and adhesion molecules was not increased in the normal group and the ischemia group.But the expression of cytokines and adhesion molecules in ischemia area after reperfusion and the infiltration of PMN were changed successively.The expression of IL-1mRNA was increased after reperfusion for2hours,which was about twice as much as that of the comparative groups.It peaked after reperfusion for6hours,and lasted to12hours.The expression of ICAM-1mRNA was increased remarkbly after reperfusion for4hours;for12hours,its fluorescent intensity on microvascular area per unit was increased about one second more than that of the ischemia group.Conclusion:The increased expression of spinal cord microvascular ICAM-1and its regulating factor IL-1βafter I/R injury is the important molecular basis causing blood spinal cord barrier injury.
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