Ucf-101对大鼠局灶性脑缺血再灌注后Caspase-3蛋白表达的影响

目的观察Ucf—101对大鼠脑缺血再灌注后神经元caspase-3蛋白表达及细胞凋亡的影响，研究其对缺血性脑损伤是否具有保护作用。方法将36只雄性WiStar大鼠随机分为3组：假手术组、缺血组及Ucf—101组，采用线栓法建立大鼠右侧大脑中动脉闭塞（middle cerebral artery occlusion，MCAO）2h再灌注模型，于再灌注后6h和24h断头取脑，采用TTC法测梗死体积，TUNEL法原位标记DNA片段，检测TUNEL阳性细胞的变化，免疫组化法观察脑皮质神经元caspase-3的表达。结果脑缺血再灌注后不同时间点（6h、24h），Ucf-101组与缺血组相比梗死体积明显缩小，有显著性差异（P〈0．05）；假手术组未见梗死现象。缺血组TUNEL阳性细胞数较假手术组明显增多（P〈0．05），脑皮质caspase-3的表达较假手术组亦显著增强（P〈0．05），给予Ucf-101处理后，TUNEL阳性细胞数较缺血组明显减少（P〈0．05），caspase-3的表达较缺血组亦明显减弱（P〈0．05）。结论Ucf-101能有效地抑制脑缺血再灌注损伤，下调脑皮质神经元Caspase-3蛋白的表达，抑制神经元的凋亡，发挥神经保护作用。

THE EFFECTS OF Uef-101 ON THE EXPRESSION OF CASPASE-3 DURING FOCAL CEREBRAL ISCHEMIA-REPERFUSION IN RATS

Objective To investigate the neuroprotective effects of Ucf-101, during cerebral ischemiareperfusion. Methods 36 male Wistar rats were randomly divided into 3 groups： sham operation group, cerebral ischemia group and Ucf-101 treatment group. The focal cerebral ischemia models of rats were established by the right middle cerebral artery occlusion（MCAO） with thread occlusion methods. Reperfusion began 2h after occlusion. After 6h and 24h of focal cerebral ischemia-reperfusion, the rats were killed and decapitated to gain brains. The infarct volumes were calculated by TTC; TUNEL was used to measure TUNEL positive neuron; the expression of Caspase-3 was detected by immunohistochemistry. Results After 6h and 24h of focal cerebral ischemia-reperfusion, Ucf-101 was decreased the infarct volume significantly when compared with the ischemia group（P〈0.05）, respectively. There was no focal ischemia in the sham group. The number of TUNEL positive neurons and the expression of caspase-3 in the ischemia group were distinctively higher than that in the sham group. In the Ucf-101 group, they were significantly decreased comparing with that of the ischemia group （P〈0.05） Conclusion Ucf-101 treatment can decrease the number of apoptotic neurons and the expression of apoptotic protein caspase-3. Ucf-101 can protect the neurons during cerebral ischemia-reperfusion.