• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

PTZ 点燃癫痫模型小鼠皮质中抗氧化蛋白 TRX1、TXNL1 和 TXNRD1 的上调。

Up-regulation of antioxidative proteins TRX1, TXNL1 and TXNRD1 in the cortex of PTZ kindling seizure model mice.

机构信息

Department of Anatomy, College of Biomedical Sciences, Xuzhou Medical University, Xuzhou, Jiangsu Province, China.

Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, Jiangsu Province, China.

出版信息

PLoS One. 2019 Jan 24;14(1):e0210670. doi: 10.1371/journal.pone.0210670. eCollection 2019.

DOI:10.1371/journal.pone.0210670
PMID:30677045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6345427/
Abstract

Oxidative stress has been considered as one of pathogenesis of brain damage led by epilepsy. Reducing oxidative stress can ameliorate brain damage during seizures. However, expression levels of important antioxidative enzymes such as thioredoxin-1 (TRX1), thioredoxin-like 1 protein (TXNL1) and thioredoxin reductase 1 (TXNRD1) during seizures have not been investigated. In this study, we examined protein and mRNA expression levels of TRX1, TXNL1 and TXNRD1 in different brain regions in PTZ induced seizure model mice. We found that protein expression levels of TRX1, TXNL1 and TXNRD1 are simultaneously up-regulated by 2- or 3-fold in the cortex of both acute and chronic seizure model mice. But there is no unified expression pattern change of these enzymes in the hippocampus, cerebellum and diencephalon in the seizure model mice. Less extent up-regulation of mRNA expression of these enzymes were also observed in the cortex of seizure mice. These data suggest that antioxidative enzymes may provide a protective effect against oxidative stress in the cortex during seizures.

摘要

氧化应激被认为是癫痫引起的脑损伤的发病机制之一。减少氧化应激可以改善癫痫发作时的脑损伤。然而,在癫痫发作期间,重要抗氧化酶如硫氧还蛋白-1(TRX1)、硫氧还蛋白样蛋白 1(TXNL1)和硫氧还蛋白还原酶 1(TXNRD1)的表达水平尚未得到研究。在这项研究中,我们检查了 PTZ 诱导的癫痫模型小鼠不同脑区中 TRX1、TXNL1 和 TXNRD1 的蛋白和 mRNA 表达水平。我们发现,TRX1、TXNL1 和 TXNRD1 的蛋白表达水平在急性和慢性癫痫模型小鼠的皮质中同时上调了 2 到 3 倍。但在癫痫模型小鼠的海马、小脑和间脑,这些酶并没有统一的表达模式变化。在癫痫小鼠的皮质中,这些酶的 mRNA 表达也有较小程度的上调。这些数据表明,抗氧化酶可能在癫痫发作时为皮质提供对抗氧化应激的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/554899401d32/pone.0210670.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/e3edd5b5a56e/pone.0210670.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/189908d48c3e/pone.0210670.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/9c2e79b3e2ff/pone.0210670.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/554899401d32/pone.0210670.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/e3edd5b5a56e/pone.0210670.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/189908d48c3e/pone.0210670.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/9c2e79b3e2ff/pone.0210670.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0930/6345427/554899401d32/pone.0210670.g004.jpg

相似文献

1
Up-regulation of antioxidative proteins TRX1, TXNL1 and TXNRD1 in the cortex of PTZ kindling seizure model mice.PTZ 点燃癫痫模型小鼠皮质中抗氧化蛋白 TRX1、TXNL1 和 TXNRD1 的上调。
PLoS One. 2019 Jan 24;14(1):e0210670. doi: 10.1371/journal.pone.0210670. eCollection 2019.
2
Decreased expression of hippocampal Na⁺/Ca²⁺ exchanger isoform-1 by pentylenetetrazole kindling in mice.戊四氮点燃小鼠致海马钠/钙交换蛋白亚型1表达降低
Epilepsy Res. 2015 Sep;115:109-12. doi: 10.1016/j.eplepsyres.2015.06.002. Epub 2015 Jun 5.
3
TXNL1 has dual functions as a redox active thioredoxin-like protein as well as an ATP- and redox-independent chaperone.TXNL1 兼具氧化还原活性硫氧还蛋白样蛋白和 ATP 及氧化还原独立伴侣这两种功能。
Redox Biol. 2023 Nov;67:102897. doi: 10.1016/j.redox.2023.102897. Epub 2023 Sep 26.
4
Activin mRNA induced during amygdala kindling shows a spatiotemporal progression that tracks the spread of seizures.杏仁核点燃过程中诱导产生的激活素信使核糖核酸呈现出一种时空进展,该进展追踪癫痫发作的传播。
J Comp Neurol. 2004 Aug 9;476(1):91-102. doi: 10.1002/cne.20197.
5
Anticonvulsant activity of an active fraction extracted from Crinum jagus L. (Amaryllidaceae), and its possible effects on fully kindled seizures, depression-like behaviour and oxidative stress in experimental rodent models.从文殊兰(石蒜科)中提取的活性成分的抗惊厥活性及其对实验性啮齿动物模型中完全点燃性癫痫发作、抑郁样行为和氧化应激的可能影响。
J Ethnopharmacol. 2016 Dec 24;194:421-433. doi: 10.1016/j.jep.2016.10.023. Epub 2016 Oct 8.
6
Epileptogenic effects of G protein-coupled estrogen receptor 1 in the rat pentylenetetrazole kindling model of epilepsy.G蛋白偶联雌激素受体1在大鼠戊四氮点燃癫痫模型中的致痫作用
Pharmacol Rep. 2016 Feb;68(1):66-70. doi: 10.1016/j.pharep.2015.07.001. Epub 2015 Jul 17.
7
The molecular evaluation of thioredoxin (TXN1 & TXN2), thioredoxin reductase 1 (TXNRd1), and oxidative stress markers in a binary rat model of hypo- and hyperthyroidism after treatment with gallic acid.探讨没食子酸处理后的甲状腺功能减退和甲状腺功能亢进症二元大鼠模型中硫氧还蛋白(TXN1 和 TXN2)、硫氧还蛋白还原酶 1(TXNRd1)和氧化应激标志物的分子评估。
Drug Chem Toxicol. 2023 Nov;46(6):1108-1115. doi: 10.1080/01480545.2022.2131812. Epub 2022 Oct 31.
8
Genetic Modulation of HSPA1A Accelerates Kindling Progression and Exerts Pro-convulsant Effects.HSPA1A 的遗传调控加速了点燃进展,并产生促惊厥作用。
Neuroscience. 2018 Aug 21;386:108-120. doi: 10.1016/j.neuroscience.2018.06.031. Epub 2018 Jun 30.
9
Oxidation of structural cysteine residues in thioredoxin 1 by aromatic arsenicals enhances cancer cell cytotoxicity caused by the inhibition of thioredoxin reductase 1.芳香族砷化合物使硫氧还蛋白 1 中的结构半胱氨酸残基氧化,增强了硫氧还蛋白还原酶 1 抑制引起的癌细胞细胞毒性。
Free Radic Biol Med. 2015 Dec;89:192-200. doi: 10.1016/j.freeradbiomed.2015.07.010. Epub 2015 Jul 11.
10
Comparative studies on the effects of clinically used anticonvulsants on the oxidative stress biomarkers in pentylenetetrazole-induced kindling model of epileptogenesis in mice.关于临床使用的抗惊厥药物对戊四氮诱导的小鼠癫痫发生点燃模型中氧化应激生物标志物影响的比较研究。
J Basic Clin Physiol Pharmacol. 2017 Jan 1;28(1):31-42. doi: 10.1515/jbcpp-2016-0034.

引用本文的文献

1
Differential Expression of Erythrocyte Proteins in Patients with Alcohol Use Disorder.酒精使用障碍患者红细胞蛋白的差异表达
Int J Mol Sci. 2025 Aug 23;26(17):8199. doi: 10.3390/ijms26178199.
2
Targeting TXN1 Induces G2M Phase Arrest and Apoptosis of Glioma Cells Through P38 MAPK Pathway.靶向TXN1通过P38丝裂原活化蛋白激酶途径诱导胶质瘤细胞的G2/M期阻滞和凋亡。
Appl Biochem Biotechnol. 2025 Aug 20. doi: 10.1007/s12010-025-05341-x.
3
Identifying dysregulated regions in amyotrophic lateral sclerosis through chromatin accessibility outliers.

本文引用的文献

1
The role of the thioredoxin/thioredoxin reductase system in the metabolic syndrome: towards a possible prognostic marker?硫氧还蛋白/硫氧还蛋白还原酶系统在代谢综合征中的作用:是否可能成为一种预后标志物?
Cell Mol Life Sci. 2018 May;75(9):1567-1586. doi: 10.1007/s00018-018-2745-8. Epub 2018 Jan 11.
2
Neuronal Nitric Oxide Synthase Contributes to PTZ Kindling Epilepsy-Induced Hippocampal Endoplasmic Reticulum Stress and Oxidative Damage.神经元型一氧化氮合酶促成戊四氮点燃癫痫诱导的海马内质网应激和氧化损伤。
Front Cell Neurosci. 2017 Nov 28;11:377. doi: 10.3389/fncel.2017.00377. eCollection 2017.
3
Redox Signaling Mediated by Thioredoxin and Glutathione Systems in the Central Nervous System.
通过染色质可及性异常值鉴定肌萎缩侧索硬化症中的失调区域。
HGG Adv. 2024 Jul 18;5(3):100318. doi: 10.1016/j.xhgg.2024.100318. Epub 2024 Jun 13.
4
Melatonin antagonizes oxidative stress-induced apoptosis in retinal ganglion cells through activating the thioredoxin-1 pathway.褪黑素通过激活硫氧还蛋白-1 通路拮抗氧化应激诱导的视网膜神经节细胞凋亡。
Mol Cell Biochem. 2024 Dec;479(12):3393-3404. doi: 10.1007/s11010-024-04924-2. Epub 2024 Feb 14.
5
Proteomic-miRNA Biomics Profile Reveals 2D Cultures of Human iPSC-Derived Neural Progenitor Cells More Sensitive than 3D Spheroid System Against the Experimental Exposure to Arsenic.蛋白质组学-miRNA 生物组学分析揭示,与人诱导多能干细胞源性神经祖细胞的 2D 培养物相比,3D 球体系统对砷的实验暴露更敏感。
Mol Neurobiol. 2024 Aug;61(8):5754-5770. doi: 10.1007/s12035-024-03924-z. Epub 2024 Jan 16.
6
Cerebral Malaria Model Applying Human Brain Organoids.应用人脑类器官的脑疟疾模型。
Cells. 2023 Mar 23;12(7):984. doi: 10.3390/cells12070984.
7
Identification of the Acid-Sensitive Site Critical for Chloral Hydrate (CH) Activation of the Proton-Activated Chloride Channel.鉴定氯醛(CH)激活质子激活氯离子通道的关键酸性敏感位点。
J Neurosci. 2023 Jan 25;43(4):526-539. doi: 10.1523/JNEUROSCI.0482-22.2022. Epub 2022 Oct 25.
8
PM10 Alters Trophoblast Cell Function and Modulates miR-125b-5p Expression.PM10 改变滋养层细胞功能并调节 miR-125b-5p 的表达。
Biomed Res Int. 2022 Jan 7;2022:3697944. doi: 10.1155/2022/3697944. eCollection 2022.
9
D-SCRIPT translates genome to phenome with sequence-based, structure-aware, genome-scale predictions of protein-protein interactions.D-SCRIPT 通过基于序列、结构感知的基因组规模的蛋白质-蛋白质相互作用预测,将基因组转化为表型。
Cell Syst. 2021 Oct 20;12(10):969-982.e6. doi: 10.1016/j.cels.2021.08.010. Epub 2021 Oct 9.
10
The role of TXNL1 in disease: treatment strategies for cancer and diseases with oxidative stress.TXNL1 在疾病中的作用:癌症和氧化应激相关疾病的治疗策略。
Mol Biol Rep. 2021 Mar;48(3):2929-2934. doi: 10.1007/s11033-021-06241-z. Epub 2021 Mar 3.
中枢神经系统中由硫氧还蛋白和谷胱甘肽系统介导的氧化还原信号传导
Antioxid Redox Signal. 2017 Nov 1;27(13):989-1010. doi: 10.1089/ars.2016.6925. Epub 2017 May 18.
4
Non-invasive imaging of the levels and effects of glutathione on the redox status of mouse brain using electron paramagnetic resonance imaging.利用电子顺磁共振成像对小鼠大脑氧化还原状态下谷胱甘肽水平及作用进行无创成像。
Biochem Biophys Res Commun. 2017 Apr 15;485(4):802-806. doi: 10.1016/j.bbrc.2017.02.134. Epub 2017 Feb 28.
5
Lithium-Responsive Seizure-Like Hyperexcitability Is Caused by a Mutation in the Voltage-Gated Sodium Channel Gene .锂反应性癫痫样过度兴奋由电压门控钠通道基因突变引起。
eNeuro. 2016 Nov 10;3(5). doi: 10.1523/ENEURO.0221-16.2016. eCollection 2016 Sep-Oct.
6
A novel mouse model for the identification of thioredoxin-1 protein interactions.一种用于鉴定硫氧还蛋白-1蛋白相互作用的新型小鼠模型。
Free Radic Biol Med. 2016 Oct;99:533-543. doi: 10.1016/j.freeradbiomed.2016.09.013. Epub 2016 Sep 14.
7
Epilepsy-Related Slack Channel Mutants Lead to Channel Over-Activity by Two Different Mechanisms.癫痫相关的Slack通道突变体通过两种不同机制导致通道过度激活。
Cell Rep. 2016 Jan 5;14(1):129-139. doi: 10.1016/j.celrep.2015.12.019. Epub 2015 Dec 24.
8
Brain redox imaging in the pentylenetetrazole (PTZ)-induced kindling model of epilepsy by using in vivo electron paramagnetic resonance and a nitroxide imaging probe.利用体内电子顺磁共振和氮氧化物成像探针,在戊四氮(PTZ)诱导的癫痫点燃模型中进行脑氧化还原成像。
Neurosci Lett. 2015 Nov 3;608:40-4. doi: 10.1016/j.neulet.2015.10.008. Epub 2015 Oct 28.
9
Mitochondrial dysfunction and seizures: the neuronal energy crisis.线粒体功能障碍与癫痫:神经元能量危机
Lancet Neurol. 2015 Sep;14(9):956-66. doi: 10.1016/S1474-4422(15)00148-9.
10
Ceruloplasmin is an endogenous protectant against kainate neurotoxicity.铜蓝蛋白是一种内源性保护剂,可对抗红藻氨酸的神经毒性。
Free Radic Biol Med. 2015 Jul;84:355-372. doi: 10.1016/j.freeradbiomed.2015.03.031. Epub 2015 Apr 2.