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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The role of microRNA-146a in regulating the expression of IRAK1 in cerebral ischemia-reperfusion injury
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The role of microRNA-146a in regulating the expression of IRAK1 in cerebral ischemia-reperfusion injury

机译：MicroRNA-146A在调节脑缺血再灌注损伤中伊拉克1表达的作用

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摘要

MicroRNA-146a (miR-146a) is reportedly implicated in the pathogenesis of ischemia-reperfusion (I/R) injury; however, its role in cerebral I/R injury is unclear and requires further investigation. In this study, cerebral I/R injury was established in mice via middle cerebral artery occlusion, and the expression of miR-146a was detected in the brain tissue via quantitative real-time PCR. We found that the expression of miR-146a was upregulated. Furthermore, the endogenous miR-146a was antagonized by its specific inhibitor. The results indicated that the inhibition of miR-146a deteriorated I/R-induced neurobehavioral impairment, exaggerated the infarct size, and exacerbated blood-brain barrier leakage. Cerebral I/R injury-induced generation of inflammatory cytokines, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6, was further promoted by miR-146a inhibitor. The expression of interleukin-1 receptor associated kinase 1 (IRAK1), a target of miR-146a, was upregulated upon miR-146a inhibition. In addition, the nuclear factor kappa B (NF-kappa B) signaling pathway was over-activated when miR-146a was antagonized as manifested by the increased levels of phospho-NF-kappa B inhibitor alpha and nuclear p65. In summary, our findings demonstrate that the elevation of miR-146a may be one of the compensatory responses after the cerebral I/R injury and suggest miR-146a as a potential therapeutic target for cerebral I/R injury.
机译：据报道，MicroRNA-146a（miR-146a）涉及缺血再灌注（I / R）损伤的发病机制;然而，它在脑I ​​/ R损伤中的作用尚不清楚，需要进一步调查。在该研究中，通过中脑动脉闭塞在小鼠中建立了脑I / R损伤，并通过定量实时PCR在脑组织中检测miR-146a的表达。我们发现miR-146a的表达被上调。此外，内源性miR-146a被其特异性抑制剂拮抗。结果表明，抑制miR-146a劣化的I / R诱导的神经障碍损伤，夸大了梗塞尺寸，加剧了血脑屏障泄漏。 MiR-146A抑制剂进一步促进了脑I / R损伤诱导的炎性细胞因子，肿瘤坏死因子（TNF） - α，白细胞介素（IL）-1和IL-6。在miR-146a抑制时上调白细胞介素-1受体相关激酶1（Irak1）的表达，MiR-146a的靶标。此外，当MiR-146a拮抗的情况下，核因子Kappa B（NF-Kappa B）信号传导途径被拮抗，如磷酸 - NF-κB抑制剂α和核P65的增加。总之，我们的研究结果表明miR-146a的升高可以是脑I / r损伤后的补偿反应之一，并提出miR-146a作为脑I / r损伤的潜在治疗靶标。

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  • 作者

    Chu Bo; Zhou Yadong; Zhai Heng; Li Lei; Sun Li; Li Yun;

  • 作者单位

    Shandong Univ Jinan Cent Hosp Dept Crit Med Jinan 250013 Shandong Peoples R China;

    Taishan Med Univ Affiliated Hosp Dept Emergency Med Tai An 271000 Shandong Peoples R China;

    Zibo Cent Hosp Dept Emergency Med Zibo 255036 Shandong Peoples R China;

    Shandong Chest Hosp Eastern Branch Dept Crit Med Jinan 250013 Shandong Peoples R China;

    Shandong Univ Jinan Cent Hosp Dept Crit Med Jinan 250013 Shandong Peoples R China;

    Shandong Univ Jinan Cent Hosp Dept Crit Med Jinan 250013 Shandong Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 药理学;
  • 关键词

    miR-146a; cerebral I/R injury; inflammatory response; IRAK1; NF-kappa B;

    机译：miR-146a;脑I / R损伤;炎症反应;伊拉克1;NF-Kappa B;

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