Role of ERK1／2 in ischemia-reperfusion injury of spinal cord
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摘要:
目的：研究细胞外信号调节激酶1／2（extracellular signal-regulated kinases1／2，ERK1／2）在脊髓缺血再灌注中的作用及机制。方法：观察不同时间段脊髓缺血再灌注标本的形态学改变，Western blot 检测脊髓标本中ERK1／2的磷酸化，免疫组织化学染色分析磷酸化ERK1／2（pERK1／2）在神经细胞内的定位表达。结果：脊髓缺血30 min／再灌注2 h ERK1／2发生磷酸化，并持续至再灌注24 h；对照组、脊髓缺血30 min／再灌注5 min至再灌注1 h，免疫组织化学染色未检测到pERK1／2在运动神经细胞内表达，脊髓缺血30 min／再灌注2 h至再灌注24 h，pERK1／2在运动神经细胞胞浆及胞核内均表达，且胞浆内表达异常显著。结论：脊髓缺血再灌注时ERK1／2发生磷酸化，pERK1／2过度滞留于细胞浆可能与脊髓缺血再灌注损伤引发的神经细胞凋亡有关。
Abstract:
Objective：To investigate the role of extracellular signal-regulated kinases1／2（ERK1／2） in inschemia-reperfusion injuty of spinal cord. Methods：The morphology of spinal cord by hematoxylin and eosin（HE） stain and electron microscope in different ischemia／reperfusion time were observed. The activation of ERK1／2（pERK1／2） was detected by western blot and the localization of pERK1／2 was analyzed by immunohistochemistry. Results：ERK1／2 was activated in spinal cord occluded for 30 min and reperfused for 2 to 24 h. No pERK1／2 was found in neurocyte in the control group by immunohistochemistry. PERK1／2 was stained both in the cytoplasm and nucleus after 30 min of occlusion and 2 h of reperfusion, and stained further after 8 to 24 h of reperfasion. Conclusion：ERK1／2 was activated in the reperfusion of ischemic spinal cord and the stagnation of pERK1／2 in the cytoplasm during reperfusion of ischemic spinal cord may lead to neurocyte apoptosis.
