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目的探讨亚低温对大鼠脑缺血再灌注损伤后谷氨酸载体兴奋性氨基酸载体(EAAC) 1mRNA表达和损伤神经细胞凋亡的影响。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30min,再灌注损伤90min,用原位杂交法和原位缺口末端标记法分别检测假手术组、对照组和亚低温组的谷氨酸载体EAAC1mRNA表达阳性率和凋亡细胞百分率。结果与对照组比较,假手术组的EAAC1mRNA表达阳性率和凋亡细胞百分率均明显降低(P<0.05和P<0.01),而亚低温组EAAC1mRNA表达阳性率显著升高(P<0.05),但凋亡细胞百分率明显下降(P<0.05)。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上调EAAC1mRNA表达、诱导EAAC1合成及增加谷氨酸的摄取有关。
Objective To investigate the effects of mild hypothermia on the expression of glutamate transporter excitatory amino acid carrier (EAAC) 1 mRNA and the injury of injured neurons after cerebral ischemia-reperfusion injury in rats. Methods The model of focal cerebral ischemia-reperfusion injury in rats was established. The middle cerebral artery occlusion was occured for 30 min and the reperfusion injury was 90 min. The in situ hybridization and in situ nick end labeling Of the glutamate vector EAAC1mRNA expression positive rate and percentage of apoptotic cells. Results Compared with the control group, the positive rate of EAAC1 mRNA and the percentage of apoptotic cells in sham operation group were significantly decreased (P <0.05 and P <0.01), while the positive rate of EAAC1 mRNA expression in hypothermia group was significantly increased (P <0.05) The percentage of apoptotic cells decreased significantly (P <0.05). CONCLUSIONS: The neuronal apoptosis induced by mild hypothermia after cerebral ischemia-reperfusion injury may be related to the up-regulation of EAAC1mRNA, induction of EAAC1 synthesis and increase of glutamate uptake.