长非编码 RNA XIST 通过下调 miR-370-3p 和调控 PI3K/AKT/mTOR 通路抑制 LPS 诱导的 AC16 细胞炎症和凋亡

IF 1.6 4区 医学 Q4 BIOCHEMICAL RESEARCH METHODS
Jun Xiao, Min Qiu, Mingzhi Long, Shushu Zhou, Shouyu Guo, Shaohua Xu, Hai Jiang
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引用次数: 0

摘要

背景/目的:心肌炎是一种严重的疾病,其特征是心脏肌肉壁发炎,从而导致青壮年猝死。长非编码 RNA X-非活性特异性转录本(LncRNA XIST)是一类长度˃ 200 nts 的转录本,不具有编码蛋白质的能力。它们在各种癌症和炎症性疾病中发挥凋亡功能:本研究旨在探讨 XIST 对 LPS 诱导的 AC16 细胞炎症的影响和机制:方法:用 LPS 刺激 AC16 细胞,建立体外炎症损伤模型。CCK-8用于检测AC16细胞的活力,FCM用于检测细胞凋亡。用 Elisa 法检测 IL-8、IL-1β 和 TNF-α 的水平。RT-qPCR 用于检测 LPS 刺激的 AC16 细胞中的 XIST、miR-370-3p、Bax 和 Bcl-2。用 Elisa 法评估 AC16 细胞中 PI3K、AKT 和 mTOR 的磷酸化情况:结果:我们的研究结果表明,暴露于 LPS 会显著降低 AC16 细胞的存活率,同时增加炎症和细胞凋亡。此外,在受到 LPS 刺激的 AC16 细胞中,XIST 的表达也有所降低。在 AC16 细胞中过表达 XIST 可提高细胞存活率,抑制细胞凋亡,并增加 Bcl-2、Bax 和炎症调节因子(IL-8、TNF-α 和 IL-1β)的表达。抑制 AC16 细胞中的 XIST 产生了相反的结果。MiR-370-3p 模拟物抑制了 XIST 对炎症、活力和细胞凋亡的影响。此外,XIST 还抑制了 LPS 损伤的 AC16 细胞中 mTOR、AKT 和 PI3K 的磷酸化水平:数据阐明了 lncRNA XIST 通过下调 miR-370-3p 和抑制 PI3K/AKT/mTOR 通路,对受 LPS 刺激的 AC16 细胞产生抗炎和抗凋亡作用。这些发现为心肌炎的治疗提供了一种新策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
WITHDRAWN: Long Non-coding RNA XIST Impedes LPS-induced AC16 Cell Inflammation and Apoptosis through Down-regulating miR-370-3p and Regulating PI3K/AKT/mTOR Pathways

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.

The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

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来源期刊
CiteScore
3.10
自引率
5.60%
发文量
327
审稿时长
7.5 months
期刊介绍: Combinatorial Chemistry & High Throughput Screening (CCHTS) publishes full length original research articles and reviews/mini-reviews dealing with various topics related to chemical biology (High Throughput Screening, Combinatorial Chemistry, Chemoinformatics, Laboratory Automation and Compound management) in advancing drug discovery research. Original research articles and reviews in the following areas are of special interest to the readers of this journal: Target identification and validation Assay design, development, miniaturization and comparison High throughput/high content/in silico screening and associated technologies Label-free detection technologies and applications Stem cell technologies Biomarkers ADMET/PK/PD methodologies and screening Probe discovery and development, hit to lead optimization Combinatorial chemistry (e.g. small molecules, peptide, nucleic acid or phage display libraries) Chemical library design and chemical diversity Chemo/bio-informatics, data mining Compound management Pharmacognosy Natural Products Research (Chemistry, Biology and Pharmacology of Natural Products) Natural Product Analytical Studies Bipharmaceutical studies of Natural products Drug repurposing Data management and statistical analysis Laboratory automation, robotics, microfluidics, signal detection technologies Current & Future Institutional Research Profile Technology transfer, legal and licensing issues Patents.
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