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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(P<0.05)。与缺血再灌注组相比,UCF-101处理组梗死体积明显缩小(P<0.05),UCF-101处理组脑组织凋亡细胞数和Caspase-9的表达均明显减少(P<0.05)。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。
Objective To investigate the effects of UCF-101 on neuronal apoptosis and the expression of Caspase-9 after cerebral ischemia-reperfusion injury in rats and the neuroprotective effect of UCF-101 on ischemic brain injury. Methods Rats were randomly divided into sham operation group, ischemia-reperfusion group and UCF-101 treatment group. The Wistar rat middle cerebral artery occlusion (MCAO) 2h reperfusion model was established by thread occlusion. The brain was taken 24 hours after reperfusion, the infarction volume was measured by TTC, the neuronal apoptosis was detected by TUNEL method, the brain tissue was observed by immunohistochemistry Expression of neuronal Caspase-9 protein. Results No infarction was observed in sham operation group. Compared with sham operation group, the number of apoptotic cells and expression of Caspase-9 in ischemia-reperfusion group were significantly increased (P <0.05). Compared with ischemia reperfusion group, infarct volume in UCF-101 group was significantly reduced (P <0.05), and the number of apoptotic cells and Caspase-9 expression in UCF-101 group were significantly decreased (P <0.05). Conclusion UCF-101 may play a neuroprotective role by down-regulating the expression of Caspase-9 protein in neurons and inhibiting neuronal apoptosis.