UCF-101对大鼠脑缺血再灌注损伤的神经保护作用

目的观察UCF-101对大鼠脑缺血再灌注损伤后神经元凋亡及Caspase-9蛋白表达的影响,探讨UCF-101对缺血性脑损伤的神经保护作用。方法随机将大鼠分为假手术组、缺血再灌注组及UCF-101处理组。采用线栓法建立Wistar大鼠大脑中动脉闭塞(MCAO)2h再灌注模型,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Caspase-9蛋白的表达。结果假手术组未见梗死现象,与假手术组比较,缺血再灌注组脑组织凋亡细胞数和Caspase-9的表达均明显升高(P0.05)。与缺血再灌注组相比,UCF-101处理组梗死体积明显缩小(P0.05),UCF-101处理组脑组织凋亡细胞数和Caspase-9的表达均明显减少(P0.05)。结论 UCF-101可能通过下调脑组织神经元Caspase-9蛋白的表达,抑制神经元的凋亡而发挥神经保护作用。

The neuroprotective effects of UCF-101 on rat focal cerebral ischemia-reperfusion

Objective To investigate the neuroprotective effects of protease inhibitor 5-5-（2-nitrophenyl） furfuryliodine]-1,3-diphenyl-2-thiobarbituric acid（UCF-101） on the regulation of neuronal apoptosis and the expression of Caspase-9 in rats during cerebral ischemia-reperfusion. Methods Rats were randomly divided into sham operated group, ischemia-reperfusion group and UCF-101 treated group. The focal cerebral ischemia models of Wistar rats were established by the right middle cerebral artery occlusion（MCAO） with thread occlusion method. 2hs after the right middle cerebral artery occlusion, reperfusion began and continued for 24h, the infarct volumes were calculated by TTC, TUNEL was used to measure apoptotic neurons; the expression of Caspase-9 was detected by immunohistochemistry. Results There was no focal ischemia in sham operated group, the number of TUNEL positive neurons and the expression of Caspase-9 were distinctively higher in ischemia-reperfusion group than in sham operated group. The infarct volume and the number of TUNEL positive neurons and the expression of Caspase-9 were significantly decreased in UCF-101 treated group compared with ischemia-reperfusion group（P0.05）. Conclusion The protective effect of UCF-101 on the neurons during the cerebral ischemia-reperfusion might be related to the decrease of the quantity of the apoptosis neurons and the expression of apoptotic protein Caspase-9.