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目的:观察病变侧缺血至再灌期亚低温(32~33℃)对局灶脑缺血再灌注后梗死体积和神经营养因子-3(neurotrophin-3,NT-3)表达的影响。方法:采用改良线栓法建立大鼠大脑中动脉缺血再灌注模型,随机分为假手术组、常温缺血组和亚低温缺血组,缺血30 min后应用负反馈控温半导体制冷块对大鼠病变侧给予亚低温治疗并持续至再灌期。处死大鼠前进行神经功能缺陷评分,氯化三苯四氮唑染色及计算机图像分析技术观察脑梗死体积,采用免疫组织化学方法检测NT-3表达,末端脱核苷酸转移酶介导的dUTP缺口标记技术观察神经细胞凋亡情况。结果:同常温缺血组相比,亚低温缺血组梗死体积明显减少,NT-3阳性细胞数量增加,凋亡的神经细胞明显减少(均P<0.05)。神经功能缺陷评分亚低温缺血组明显低于相应时间点常温缺血组(P<0.05或P<0.01)。结论:病变侧亚低温可通过增加脑缺血后NT-3的表达水平,抑制细胞凋亡而发挥脑保护作用。
Objective: To observe the effect of mild hypothermia (32 ~ 33 ℃) on the infarct volume and the expression of neurotrophin-3 (NT-3) after focal ischemia-reperfusion in rats with lesion ischemia. Methods: The model of middle cerebral artery occlusion (MCAO) in rats was established by modified suture method. The rats were randomly divided into sham operation group, normal temperature ischemia group and mild hypothermia ischemia group. After 30 min of ischemia, Mild hypothermia was given to the lesion in rats and continued until reperfusion. Neurological deficit score, chlorinated tribenzotriazole staining and computer image analysis were used to observe the volume of cerebral infarction. The expression of NT-3 was detected by immunohistochemistry, and the expression of terminal deoxynucleotidyl transferase mediated dUTP Notch labeling technique was used to observe the apoptosis of nerve cells. Results: Compared with the normal warm ischemia group, the volume of NT-3 positive cells and the number of apoptotic neurons in the mild hypothermia group were significantly decreased (all P <0.05). Neurological deficit scores were significantly lower in hypothermia ischemic group than in warm ischemia group at the corresponding time points (P <0.05 or P <0.01). Conclusion: Mild hypothermia can exert cerebral protective effects by increasing the expression of NT-3 after cerebral ischemia and inhibiting apoptosis.