苏丹颖 吴海云 吕曼华 张丽 孙菲菲 高冠群 杨子超.UCF-101 对大鼠局灶性脑缺血再灌注后JNK和ERK活性的影响[J].,2015,15(19):3613-3615 |
UCF-101 对大鼠局灶性脑缺血再灌注后JNK和ERK活性的影响 |
The Effect of UCF-101 on the Activation of JNK and ERK after FocalCerebral Ischemia-reperfusion Injury in Rats |
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DOI: |
中文关键词: UCF-101 脑缺血再灌注 胞外信号调节酶 c-Jun 氨基末端激酶 |
英文关键词: UCF-101 Cerebral ischemia-reperfusion ERK JNK |
基金项目:黑龙江省教育厅科学技术研究项目(12511255) |
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中文摘要: |
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。 |
英文摘要: |
Objective:To investigate the neuroprotective effect of 5- [5- (2-nitrophenyl)furfuryliodine]-1,3-diphenyl-2-
thiobarbituric acid (UCF-101) on activation of C-Jun NH2-terminal kinases (JNK) and extracelluar-regulated protein kinases (ERK) after
cerebral ischemia-reperfusion injury in rats.Methods:The focal cerebral ischemia models of Wistar rats were established by the right
middle cerebral artery occlusion (MCAO) with thread occlusion methods. Reperfusion began 1h after the right middle cerebral artery
occlusion. Rats were randomly divided into sham operated group, ischemia-reperfusion group and UCF-101 treated group. Brain infarct
volume was assessed by 2, 3, 5-triphenyl tetrazolium chloride and TUNEL staining was utilized to evaluate the amount of apoptosis. In
addition, expressions of protein JNK and ERK were examined by Western blot analysis.Results:UCF-101 treatment significantly
decreased cerebral infarct size and TUNEL-positive cells in hippocampus neurons. Furthermore, UCF-101 treatment decreased JNK and
increased ERK expression.Conclusion:UCF-101 treatment has neuroprotective effects against cerebral ischemia-reperfusion injury in
rats, and that this may be associated with differentialy regulation of ERK and JNK expression. |
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