Silencing lncRNA GABPB1-AS1 alleviates cerebral ischemia reperfusion injury through the miR-641/NUCKS1 axis.

IF 16.4 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY

Accounts of Chemical Research Pub Date : 2024-07-15 eCollection Date: 2024-01-01 DOI:10.62347/EAGK7098

Shui Yu, Zhangming Zhou, Zhang Liang, Chenbin Ruan, Lei Bai, Ying Pi

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引用次数: 0

Abstract

Objective: To investigate the possible mechanism of lncRNA GA binding protein transcription factor beta subunit 1 antisense RNA 1 (GABPB1-AS1) in cerebral ischemia/reperfusion (CI/R) injury.

Methods: RT-qPCR was applied to determine GABPB1-AS1 expression in oxygen-glucose deprivation/reoxygenation (OGD/R) cells. The targeting relationships between GABPB1-AS1 and miR-641, as well as between miR-641 and nuclear casein and cyclin-dependent kinase substrate 1 (NUCKS1) were examined by dual luciferase reporter assay. The protein expression of caspase-3, Bax, Bcl-2 and NUCKS1 was examined by western blot. Cell apoptosis was measured by flow cytometry (FCM) and western blot. Cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.

Results: GABPB1-AS1 was significantly elevated in SH-SY5Y cells under OGD/R. Downregulation of GABPB1-AS1 accelerated cell viability and suppressed cell apoptosis. GABPB1-AS1 silencing reduced ROS and MDA levels in OGD/R-treated cells. Furthermore, miR-641 inhibitor aggravated damage from OGD/R, but GABPB1-AS1 silencing notably attenuated this effect. NUCKS1 was proven to be a target gene of miR-641.

Conclusion: GABPB1-AS1 silencing alleviated CI/R injury through the miR-641/NUCKS1 axis, indicating that GABPB1-AS1 might serve as a therapeutic target for CI/R injury.

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沉默lncRNA GABPB1-AS1可通过miR-641/NUCKS1轴减轻脑缺血再灌注损伤

目的研究lncRNA GA结合蛋白转录因子β亚基1反义RNA 1（GABPB1-AS1）在脑缺血再灌注（CI/R）损伤中的可能机制：方法：应用 RT-qPCR 技术检测 GABPB1-AS1 在氧-葡萄糖剥夺/复氧（OGD/R）细胞中的表达。通过双荧光素酶报告实验检测了 GABPB1-AS1 与 miR-641 之间的靶向关系，以及 miR-641 与核酪蛋白和细胞周期蛋白依赖性激酶底物 1（NUCKS1）之间的靶向关系。通过 Western 印迹检测了 caspase-3、Bax、Bcl-2 和 NUCKS1 的蛋白表达。细胞凋亡通过流式细胞术（FCM）和蛋白印迹进行检测。细胞活力通过 3-（4,5-二甲基噻唑-2-基）-2,5-二苯基溴化四氮唑（MTT）检测法进行评估：结果：在OGD/R条件下，GABPB1-AS1在SH-SY5Y细胞中明显升高。下调 GABPB1-AS1 可提高细胞活力并抑制细胞凋亡。沉默 GABPB1-AS1 可降低 OGD/R 处理细胞中的 ROS 和 MDA 水平。此外，miR-641抑制剂会加重OGD/R造成的损伤，但GABPB1-AS1沉默会显著减轻这种影响。NUCKS1 被证明是 miR-641 的靶基因：结论：沉默 GABPB1-AS1 可通过 miR-641/NUCKS1 轴减轻 CI/R 损伤，表明 GABPB1-AS1 可作为 CI/R 损伤的治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.