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目的观察亚低温处理大鼠脑缺血再灌注损伤后缺血侧脑组织细胞间黏附分子-1(intercellularadhesionmolecule-1,ICAM-1)的表达变化,探讨与损伤神经细胞凋亡的关系。方法采用大鼠局灶性脑缺血再灌注损伤模型,大脑中动脉阻塞2h,再灌注损伤12h,用原位缺口末端标记(TUNEL)法、反转录聚合酶链反应(RT-PCR)技术和斑点印迹杂交(Dotblotting)法分别检测假手术组、对照组和亚低温组缺血侧脑组织凋亡细胞百分率、ICAM-1mRNA和ICAM-1蛋白表达水平。结果对照组缺血侧脑组织ICAM-1mRNA、ICAM-1蛋白表达水平和凋亡细胞百分率明显高于假手术组;亚低温组缺血侧脑组织ICAM-1mRNA、ICAM-1蛋白表达水平和凋亡细胞百分率较对照组明显降低。结论亚低温的抗脑缺血再灌注损伤后损伤神经细胞凋亡作用可能与其下调缺血侧脑组织ICAM-1表达有关。
Objective To investigate the expression of intercellular adhesion molecule-1 (ICAM-1) in ischemic brain tissue after focal cerebral ischemia-reperfusion injury in mild hypothermia rats and to explore the relationship with the apoptosis of injured nerve cells. Methods The model of focal cerebral ischemia-reperfusion injury in rats was established. The middle cerebral artery was blocked for 2 hours and reperfusion injury was performed for 12 hours. TUNEL and RT-PCR And Dot blotting method were used to detect the percentage of apoptotic cells, the expression of ICAM-1mRNA and ICAM-1 in ischemic brain tissue of sham operation group, control group and mild hypothermia group respectively. Results The expression of ICAM-1 mRNA and ICAM-1 protein and the percentage of apoptotic cells in the ischemic brain tissue in the control group were significantly higher than those in the sham operation group. The expressions of ICAM-1 mRNA and ICAM-1 protein in the ischemic brain tissue in the hypothermia group The percentage of dead cells was significantly lower than that of the control group. Conclusion The neuronal apoptosis induced by mild hypothermia after cerebral ischemia-reperfusion injury may be related to the down-regulation of ICAM-1 expression in ischemic brain.