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目的观察UCF-101对大鼠脑缺血再灌注损伤后神经元凋亡及凋亡抑制蛋白XIAP表达的影响,探讨UCF-101对缺血性脑损伤的神经保护作用。方法采用线栓法建立Wistar大鼠大脑中动脉闭塞(MCAO)2h再灌注模型,随机将大鼠分为假手术组、缺血再灌注组及UCF-101处理组,于再灌注后24h取脑,采用TTC法测梗死体积,TUNEL法检测神经元凋亡,免疫组化法观察脑组织神经元XIAP蛋白的表达。结果假手术组未见梗死现象,偶见凋亡神经细胞,神经元中可见棕黄色XIAP颗粒散在分布于核膜周围胞浆中。与假手术组比较,缺血再灌注组可见梗死灶,脑组织凋亡细胞数明显增加,XIAP的表达明显降低(P<0.05);与缺血再灌注组比较,UCF-101处理组梗死体积明显缩小(P<0.05),脑组织凋亡细胞数减少,XIAP的表达均明显增加(P<0.05)。结论 UCF-101神经保护作用可能与上调脑组织神经元XIAP蛋白的表达和抑制神经元的凋亡有关。
Objective To investigate the effect of UCF-101 on neuronal apoptosis and XIAP expression after cerebral ischemia-reperfusion injury in rats and the neuroprotective effect of UCF-101 on ischemic brain injury. Methods The model of middle cerebral artery occlusion (MCAO) in Wistar rats was established by reperfusion for 2 hours. The rats were randomly divided into sham-operation group, ischemia-reperfusion group and UCF-101 treatment group. The infarct volume was measured by TTC method. Neuronal apoptosis was detected by TUNEL method. The expression of XIAP protein was detected by immunohistochemistry. Results There was no infarction in the sham operation group. Occasionally apoptotic nerve cells were found in the neurons. The brown granules of XIAP scattered in the cytoplasm around the nuclear membrane. Compared with the sham-operation group, infarct size was found in the ischemia-reperfusion group, the number of apoptotic cells in brain tissue was significantly increased, and the expression of XIAP was significantly decreased (P <0.05). Compared with the ischemia-reperfusion group, the infarct volume (P <0.05). The number of apoptotic cells in brain tissue decreased and the expression of XIAP increased significantly (P <0.05). Conclusion The neuroprotection of UCF-101 may be related to the up-regulation of XIAP protein expression and neuronal apoptosis.