Effect of UCF-101 on the JNK signal pathway during focal cerebral ischemia-reperfusion in rats
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.
Keywords：UCF-101Cerebral ischemia-reperfusionp-JNK
Publication Date：2015-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：4( 445-448 )