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目的 :观察大鼠脑缺血再灌注后不同时间缺血区细胞间粘附分子 1(ICAM 1)的表达和中性粒细胞的浸润以及神经细胞的损伤情况。方法 :40只 Wistar大鼠分为对照组、假手术组和缺血 2小时再灌注 2、4、12、2 4、48、96小时组 ,分别用免疫组织化学和组织切片方法检测大脑中动脉阻塞 2小时再灌注不同时间点局部脑组织 ICAM 1蛋白表达及中性粒细胞浸润情况。结果 :大鼠脑缺血再灌注 2小时局部脑组织 ICAM 1的表达开始升高 ,于再灌注 48小时达到峰值 ,持续至再灌注 96小时仍保持较高水平表达 ;局部缺血区域中性粒细胞浸润于再灌注后 12小时开始升高 ,48小时达到高峰 ,与 ICAM 1的表达呈同步改变。结论 :脑缺血再灌注后表达增高的 ICAM 1与局部缺血区中性粒细胞的浸润密切相关 ,这一过程是导致缺血再灌注损伤的一个重要机制
Objective: To observe the expression of intercellular adhesion molecule - 1 (ICAM - 1) and the infiltration of neutrophils and the damage of nerve cells in ischemic area of rats after cerebral ischemia - reperfusion. Methods: Forty Wistar rats were divided into control group, sham operation group, and reperfusion 2, 4, 2, 2, 4, 48, and 96 hours after ischemia for 2 hours. Immunohistochemistry and histological sections were used to detect the middle cerebral artery ICAM-1 protein expression and neutrophil infiltration in local brain tissue at 2 h after reperfusion were observed. Results: The expression of ICAM-1 in local brain began to increase 2 hours after cerebral ischemia-reperfusion in rats and peaked at 48 hours after reperfusion, and remained high until 96 hours after reperfusion. Neutrophils in ischemic area Cell infiltration began to increase 12 hours after reperfusion, peaked at 48 hours, and ICAM 1 expression changed synchronously. CONCLUSION: ICAM 1, which is increased after cerebral ischemia-reperfusion, is closely related to the infiltration of neutrophils in ischemic area. This process is an important mechanism leading to ischemia-reperfusion injury