...
首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Activation of ERK5 is mediated by N-methyl-D-aspartate receptor and L-type voltage-gated calcium channel via Src involving oxidative stress after cerebral ischemia in rat hippocampus.
【24h】

Activation of ERK5 is mediated by N-methyl-D-aspartate receptor and L-type voltage-gated calcium channel via Src involving oxidative stress after cerebral ischemia in rat hippocampus.

机译:ERK5的激活是由N-甲基-D-天冬氨酸受体和L型电压门控的钙通道经由Src介导的,涉及大鼠海马脑缺血后的氧化应激。

获取原文
获取原文并翻译 | 示例
           

摘要

Activation (phosphorylation) and the possible mechanism of extracellular signal-regulated kinase 5 (ERK5) were evaluated after cerebral ischemia-reperfusion (I/R) in the hippocampus in a four-vessel occlusion model of Sprague-Dawley rats. Western blotting showed that ERK5 was strongly activated from 10 min to 1 day and peaked at 30 min of reperfusion after 15 min ischemia. Pretreatment with N-acetylcysteine, a free radical scavenger, effectively inhibited ERK5 activation in a dose-dependent manner. Consistently, ERK5 activation was significantly suppressed by genistein (protein-tyrosine kinase inhibitor), PP2 (specific inhibitor of Src family kinases), nifedipine (L-VGCC blocker) and dextromethorphan (NMDA receptor antagonist), but not 6,7-dinitroquinoxaline-2, 3(1H, 4H)-dione (AMPA receptor antagonist). These results suggested that ERK5 could be significantly activated by I/R, which might be mediated by NMDA receptor and L-VGCC through Src kinase pathway involving oxidative stress in rat hippocampus.
机译:在Sprague-Dawley大鼠的四血管阻塞模型中,对海马脑缺血-再灌注(I / R)后,评估了激活(磷酸化)和细胞外信号调节激酶5(ERK5)的可能机制。 Western blotting显示,ERK5在10分钟至1天被强烈激活,在缺血15分钟后再灌注30分钟达到峰值。用N-乙酰半胱氨酸(一种自由基清除剂)进行的预处理以剂量依赖的方式有效抑制ERK5活化。一致地,金雀异黄酮(蛋白酪氨酸激酶抑制剂),PP2(Src家族激酶的特异性抑制剂),硝苯地平(L-VGCC阻滞剂)和右美沙芬(NMDA受体拮抗剂)显着抑制了ERK5的活化,但6,7-二硝基喹喔啉-不明显2,3(1H,4H)-二酮(AMPA受体拮抗剂)。这些结果表明,ERK5可以被I / R显着激活,这可能是由NMDA受体和L-VGCC通过Src激酶途径介导的,涉及大鼠海马的氧化应激。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号