【摘要】 目的 观察UCF-101对局灶性脑缺血-再灌注大鼠p-JNK表达的影响,探讨UCF-101对局灶性脑缺血-再灌注损伤脑保护作用的机制。方法 采用线栓法建立Wistar大鼠右侧大脑中动脉闭塞(MCAO)模型,随机分为假手术组、模型组和UCF-101组,应用2%红四唑蓝(TTC)法检测大鼠脑梗死体积,原位细胞检测(TUNEI)法检测神经元凋亡,免疫组化法及免疫印迹法(Western blot)检测脑皮层神经元p-JNK蛋白的表达。结果 UCF-101能减小大鼠脑缺血-再灌注后的脑梗死体积,减少神经细胞凋亡(P<0.05)。与假手术组比较,模型组p-JNK的表达水平增加,与模型组比较,UCF-101组能降低p-JNK的表达水平(P<0.05)。结论 UCF-101对脑缺血-再灌注损伤的保护机制可能与抑制JNK信号通路有关。更多还原

【Abstract】 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 right 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.The rats were evaluated for infarct volume by TTC staining and TUNEL method was used to measure apoptotic neurons,the expression levels of JNK phosphorylation were detected by immunohistochemistry and Western blotting analysis.Results UCF- 101 treatment significantly decreased infarct volume and reduced TUNEL positive cells in the cerebral cortex(P <0.05).Furthermore,the phosphorylation levels of JNK(p- JNK) were increased in ischemia reperfusion group than those in sham operated group.In UCF- 101 treated group the level of p- JNK decreased comparing with that in the ischemia reperfusion group(P < 0.05).Conclusion JNK signal pathway might be involved in the neuroprotective effect of UCF- 101 treatment on focal ischemic brain in rats.更多还原