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目的:探讨UCF-101对局灶性脑缺血再灌注大鼠脑内c-Jun氨基末端激酶(JNK)和胞外信号调节酶(ERK)活性的影响,进一步探讨UCF-101对局灶性脑缺血再灌注损伤脑保护作用的机制。方法:采用大脑中动脉线栓法(MCAO)建立大鼠局灶性脑缺血再灌注模型,随机分为假手术组,缺血再灌注组,UCF组,应用TTC检测大鼠脑梗死体积,TUNEL法检测神经元凋亡,Western blot检测ERK和JNK的活性。结果:UCF-101可下调脑缺血再灌注大鼠脑组织JNK蛋白的活性,上调ERK蛋白的活性,并降低梗死体积、坏死和凋亡细胞数。结论:UCF-101对大鼠局灶性脑缺血再灌注损伤有保护作用,抑制JNK凋亡通路、促进ERK生存通路,从而减轻细胞凋亡是其脑保护机制之一。
Objective: To investigate the effect of UCF-101 on the activity of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) in the brain of focal cerebral ischemia-reperfusion rats and further explore the influence of UCF- Mechanism of cerebral protection after cerebral ischemia reperfusion injury. Methods: The model of focal cerebral ischemia-reperfusion in rats was established by middle cerebral artery occlusion (MCAO). The rats were randomly divided into sham operation group, ischemia-reperfusion group and UCF group. The infarct volume, Neuronal apoptosis was detected by TUNEL method. The activity of ERK and JNK was detected by Western blot. Results: UCF-101 could down-regulate the activity of JNK protein, up-regulate the activity of ERK protein and decrease the infarction volume, necrosis and apoptotic cells in cerebral ischemia-reperfusion rats. CONCLUSION: UCF-101 has a protective effect on focal cerebral ischemia-reperfusion injury in rats, inhibits JNK apoptosis pathway, promotes ERK survival pathway and thus reduces apoptosis.