大鼠局灶性脑缺血再灌注后磷酸化细胞外信号调节激酶表达的变化

The expression of phosphorylated extracellular signal-regulated kinase followed Focal Cerebral Ischemia/Reperfusion

目的研究细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)在局灶性脑缺血再灌注中的作用。方法制备大鼠局灶性脑缺血再灌注模型,据Longa's的5级标准评分法进行神经功能评分,用免疫组织化学方法检测磷酸化ERK的表达,TUNEL染色检测神经元凋亡。结果在假手术组未检测到磷酸化的ERK表达,再灌注1h开始检测到阳性表达,再灌注4h达到峰值,12h下降;假手术组高倍镜视野仅见个别凋亡细胞,阴性对照片未检出阳性细胞,再灌注1h阳性细胞增加不明显,4h开始有明显的阳性细胞增加,24h细胞凋亡达到高峰,48h下降;磷酸化ERK阳性细胞计数与凋亡细胞数的相关分析显示相关系数(r)为-0.036,P=0.863,无统计学意义。结论局灶性脑缺血再灌注后磷酸化ERK表达增加,但其表达可能与神经元凋亡无关。

Objective To investigate the effects of phosphorylated extracellular signal-regulated kinase （P-ERK） in focal cerebral ischemia/reperfusion. Methods Transient middle cerebral artery occlusion model was subjected in Sprague-Dawley rats. The P-ERK was detected by immunohistochemistry with specific anti-bodies. The neuronal apoptosis was detected by TUNEL Apoptosis Detection Kit. Results The P-ERK positive cells were firstly observed 1 hour after reperfusion, and reached peak in 4 hours after ischemia, then declined. The TUNEL positive cells were hardly found in the brain tissue of sham operation group. More TUNEL positive cells could be found in peri-infarction 12 hours after ischemia, and the apoptosis cell counting reached peak value by the time of 24 hours after ischemia. Correlative analysis showed that no correlation between P-ERK and neuronal apoptosis （P〉0.05）. Conclusions The expression of P-ERK increases followed focal cerebral ischemia/reperfusion which may not relate to neuronal apoptosis.