目的：探讨UCF-101在大鼠脑缺血再灌注损伤中的作用及分子机制。方法采用线栓法建立Wistar大鼠大脑中动脉闭塞（ middle cerebral arteryocclusion ， MCAO）模型，随机分为假手术组、缺血再灌注组和UCF-101组，术后观察神经功能缺损症状，TUNEL法检测神经元凋亡，免疫组化法及 Western blot 检测脑皮层神经元磷酸化 p38丝裂原活化蛋白激酶（ mitogen activated protein kinase ， MAPK）蛋白的表达。结果 UCF-101改善大鼠脑缺血再灌注后的神经功能缺损症状，减少细胞凋亡（P＜0．05）；与假手术组比较，大鼠缺血后磷酸化p38 MAPK表达水平增加；与脑缺血组比较，UCF-101组磷酸化p38 MAPK表达水平有所降低（ P＜0．05）。结论UCF-101对脑缺血再灌注损伤有保护作用，其机制可能与p38 MAPK信号通路有关。%Objective To investigate the neuroprotective effect and mechanisms of 5 -[5-(2-nitrophenyl)furfuryliodine]-1,3-diphenyl-2-thiobarbituric acid (UCF-101) on the cerebral neurons of rats during cerebral ischemia -reperfusion.Methods The focal cerebral ischemia models of Wistar rats were established by the middle cerebral artery occlusion ( MCAO ) with thread occlusion methods .Rats were randomly divided into sham operated group , ischemia -reperfusion group and UCF-101 treated group .24 h after focal cerebral ischemia -reperfusion , the rats were evaluated for neurological deficits and TUNEL method was used to measure apoptotic neurons , and the expression levels of p38 MAPK phosphorylation were detected by immunohistochemistry and Western blot analysis . Results UCF -101 treatment significantly improved neurological behavior and reduced TUNEL -positive cells in the cerebral cortex . Furthermore , the phosphorylation levels of p 38 MAPK were increased in ischemia-reperfusion group thanthose in sham operated group (P<0.05).In UCF-101 treated group the phosphorylation levels of p 38 MAPK was decreased compared with the ischemia -reperfusion group ( P <0 .05 ) . Conclusion p38 MAPK signal pathway might be involved in neuroprotective effect of UCF -101 treatment on focal ischemic brain of mice .
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