کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9422670 | 1613743 | 2018 | 44 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Glutathione peroxidase 4 participates in secondary brain injury through mediating ferroptosis in a rat model of intracerebral hemorrhage
ترجمه فارسی عنوان
گلوتاتیون پراکسیداز 4 در آسیب ثانویه مغزی به وسیله میانجیگری فروپوتوز در یک مدل رت از خونریزی داخل مغزی
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کلمات کلیدی
TrxNQO1Hemeoxygenase-1GSHGSTRCDHO-1GPx4SbiROS - ROSSecondary brain injury - آسیب مغزی ثانویهSprague–Dawley - اسپراگ داولیthioredoxin - تیرودوکسینintracerebral hemorrhage - خونریزی داخل مغزیCNS - دستگاه عصبی مرکزیSOD - سدBBB - سد خونی مغزیSuperoxide dismutase - سوکسوکس دیسموتازcentral nervous system - سیستم عصبی مرکزیFerroptosis - فروتوزیسlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH Blood-brain barrier - مانع خون مغزیcerebro-spinal fluid - مایع مغزی نخاعیCSF - مایع مغزی نخاعیregulated cell death - مرگ سلولی تنظیم شده استICH - منGlutathione - گلوتاتیونglutathione-S-transferase - گلوتاتیون S-ترانسفرازglutathione peroxidase 4 - گلوتاتیون پراکسیداز 4Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Oxidative stress plays an important role in secondary brain injury (SBI) after intracerebral hemorrhage (ICH), but the underling mechanism has not been fully elucidated. Recently, the antioxidant enzyme glutathione peroxidase 4 (GPX4), has attracted increasing attention due to its ability to degrade reactive oxygen species (ROS) which are the major indicator of oxidative stress; However, the role of GPX4 in ICH has not been reported. This study was designed to investigate the changes in protein levels, as well as potential role and mechanism of GPX4 in SBI following ICH using a Sprague-Dawley (SD) rat model of ICH induced by autologous blood injection into the right basal ganglia. Firstly, GPX4 protein levels in the brain were reduced gradually and bottomed out at 24â¯h after ICH, compared with the Sham group. Secondly, genetic-overexpression of GPX4 effectively increased level of GPX4 in the brain, and clearly relieved neuronal dysfunction, brain edema, blood brain barrier (BBB) injury, oxidative stress and inflammation after ICH. In contrast, inhibiting GPX4 with a specific pharmacological inhibitor or genetic knockdown exacerbated SBI after ICH. Finally, Ferrostatin-1, a chemical inhibitor of ferroptosis, was used to explore the role of ferroptosis in brain injury after ICH. The results suggest that inhibiting ferroptosis can significantly alleviate SBI after ICH. In summary, our work indicated that GPX4 contributes to SBI following ICH by mediating ferroptosis. Therefore, inhibiting ferroptosis with specific inhibitors or upregulation of GPX4 may be a potential strategy to ameliorate brain injury induced by ICH.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1701, 15 December 2018, Pages 112-125
Journal: Brain Research - Volume 1701, 15 December 2018, Pages 112-125
نویسندگان
Zhuwei Zhang, Yu Wu, Shuai Yuan, Peng Zhang, Juyi Zhang, Haiying Li, Xiang Li, Haitao Shen, Zhong Wang, Gang Chen,