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首页> 外文期刊>Brain injury: BI >Regulation of endoplasmic reticulum stress in rat cortex by p62/ZIP through the Keap1-Nrf2-ARE signalling pathway after transient focal cerebral ischaemia
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Regulation of endoplasmic reticulum stress in rat cortex by p62/ZIP through the Keap1-Nrf2-ARE signalling pathway after transient focal cerebral ischaemia

机译：通过Keap1-NRF2通过Keap1-NRF2通过Keap1-NRF2通过Keap1-NRF2的对大鼠皮层中的内质网胁迫调节 - 在瞬态焦点脑缺血后的信号通路

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摘要

Primary objective: p62/ZIP as the autophagy receptor can transport the misfolded proteins to a macroautophagy-lysosome system for degradation and also create a positive feedback loop between p62/ZIP and Nrf2. However, the role of p62/ZIP on cerebral ischaemia is unclear. The aim of this study was to evaluate the role of p62/ZIP in the regulation of endoplasmic reticulum(ER) stress induced by cerebral ischaemia/reperfusion. Research design: Different ischemic periods were designed by transient middle cerebral artery occlusion (tMCAO) using the suture method. Methods and procedures: At 24 hours after reperfusion, the ischaemic brain tissue was studied histologically and biochemically for autophagic, ER stress and Keap1-Nrf2-ARE signalling pathway markers. Main outcomes and results: Prolongation of ischaemia significantly increased the cortical injury observed in rats and was associated with a gradual increase in the protein expression of ubiquitin-aggregates, Grp78, GADD153/CHOP and p62/ZIP. Autophagy marker Atg12-Atg5 and LC3-PE increased and then decreased. Moreover, p62/ZIP mRNA expression increased and then decreased and was consistent with Nrf2 activation. Conclusions: p62/ZIP not only plays a key role in scavenging protein aggregates during autophagy, but it may also be involved in preventing oxidative injury and alleviating ER stress through the Keap1-Nrf2-ARE signalling pathway during cerebral ischaemia/reperfusion injury.
机译：主要目的：P62 / Zip作为自噬受体可以将错误折叠的蛋白质传送到大型疏菌溶酶体系统中，用于降解，并且还在P62 / ZIP和NRF2之间产生正反馈环。然而，P62 /拉链对脑缺血的作用尚不清楚。本研究的目的是评估p62 / zip在脑缺血/再灌注诱导的内质网（ER）应激调节中的作用。研究设计：使用缝合方法的瞬时中间脑动脉闭塞（TMCAO）设计了不同的缺血时期。方法和程序：再灌注后24小时，在组织学上进行缺血性脑组织，用于自噬，ER应激和Keap1-NRF2是信号传导途径标记。主要结果和结果：血症的延长显着增加了大鼠的皮质损伤，与泛素聚集体，GRP78，GADD153 / Chec和P62 /拉链的蛋白质表达逐渐增加。自噬标记ATG12-ATG5和LC3-PE增加，然后减少。此外，P62 / Zip mRNA表达增加，然后降低，并与NRF2活化一致。结论：P62 /拉链不仅在自噬在清除蛋白质聚集体中起关键作用，但也可以参与预防氧化损伤并通过Keap1-NRF2的脑缺血/再灌注损伤期间的信号通路来减轻ER应力。

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  • 来源
    《Brain injury: BI》 |2013年第8期|共10页
  • 作者

    WangW.; KangJ.; LiH.; SuJ.; WuJ.; XuY.; YuH.; XiangX.; YiH.; LuY.; SunL.;

  • 作者单位

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Neurology First Hospital Jilin University Changchun Jilin 130021 China;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

    Department of Pathophysiology Norman Bethune College of Medicine Jilin University 126 Xinmin;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 头部及神经外科学;
  • 关键词

    Autophagy; Endoplasmic reticulum stress; Keap1; Nrf2; Oxidative stress; P62/ZIP; Transient focal cerebral ischaemia.;

    机译：自噬;内质网胁迫;Keap1;NRF2;氧化应激;p62 / zip;瞬时焦致性脑缺血。;

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