Silencing of Long noncoding RNA SOX2-OT relieves myocardial ischemia/reperfusion injury through up-regulating microRNA-146a-5p.

IF 1.5 4区医学 Q2 MEDICINE, GENERAL & INTERNAL

Bratislava Medical Journal-Bratislavske Lekarske Listy Pub Date : 2023-01-01 DOI:10.4149/BLL_2023_022

Zhongxin Li, Guangdong Liu, Hua Huang

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引用次数: 0

Abstract

Purpose: Long noncoding RNAs (lncRNAs) are involved in the development of myocardial ischemia/reperfusion injury (MIRI). In this study, we aimed to explore the regulatory effect and mechanism of lncRNA SOX2-OT in MIRI.

Methods: The expression levels of SOX2-OT and miR-146a-5p in OGD/R-treated H9C2 cells and in myocardial tissues of MIRI rats were measured by qRT-PCR. Cell viability was detected by MTT assay. The levels of IL-1β, IL-6, TNF-α, MDA, and SOD were measured by ELISA. The target relationship between SOX2-OT and miR-146a-5p was predicted by LncBase, and subsequently confirmed by DLR assay. The effects of SOX2-OT silencing on myocardial apoptosis and function were further validated in MIRI rats.

Results: The expression of SOX2-OT was increased in OGD/R-treated H9C2 cells and myocardial tissues of MIRI rats. Silencing of SOX2-OT increased the viability and inhibited the inflammation and oxidative stress of OGD/R-treated H9C2 cells. SOX2-OT negatively regulated its target miR-146a-5p. Inhibition of miR-146a-5p reversed the effects of sh-SOX2-OT on increasing the viability, and on inhibiting the inflammation and oxidative stress of OGD/R-treated H9C2 cells. In addition, silencing of SOX2-OT alleviated myocardial apoptosis and improved myocardial function in MIRI rats.

Conclusions: Silencing of SOX2-OT relieved the apoptosis, inflammation, and oxidative stress of myocardial cells via up-regulating miR-146a-5p, contributing to the remission of MIRI (Fig. 28, Ref. 33).

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长链非编码RNA SOX2-OT沉默通过上调microRNA-146a-5p减轻心肌缺血/再灌注损伤。

目的:长链非编码rna (lncRNAs)参与心肌缺血再灌注损伤(MIRI)的发生发展。在本研究中，我们旨在探讨lncRNA SOX2-OT在MIRI中的调控作用及机制。方法:采用qRT-PCR方法检测OGD/ r处理的H9C2细胞和MIRI大鼠心肌组织中SOX2-OT和miR-146a-5p的表达水平。MTT法检测细胞活力。ELISA法检测各组大鼠血清IL-1β、IL-6、TNF-α、MDA、SOD水平。通过lnbase预测SOX2-OT与miR-146a-5p之间的靶标关系，随后通过DLR检测证实。在MIRI大鼠中进一步验证SOX2-OT沉默对心肌细胞凋亡和功能的影响。结果:SOX2-OT在OGD/ r处理的MIRI大鼠H9C2细胞和心肌组织中表达升高。SOX2-OT的沉默提高了OGD/ r处理的H9C2细胞的活力，抑制了炎症和氧化应激。SOX2-OT负性调控其靶标miR-146a-5p。抑制miR-146a-5p逆转了sh-SOX2-OT提高OGD/ r处理的H9C2细胞活力、抑制炎症和氧化应激的作用。此外，SOX2-OT沉默可减轻MIRI大鼠心肌凋亡，改善心肌功能。结论:SOX2-OT的沉默通过上调miR-146a-5p减轻心肌细胞的凋亡、炎症和氧化应激，有助于MIRI的缓解(图28,Ref. 33)。

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

Bratislava Medical Journal-Bratislavske Lekarske Listy 医学-医学：内科

CiteScore

2.60

自引率

0.00%

发文量

185

审稿时长

3-8 weeks

期刊介绍： The international biomedical journal - Bratislava Medical Journal – Bratislavske lekarske listy (Bratisl Lek Listy/Bratisl Med J) publishes peer-reviewed articles on all aspects of biomedical sciences, including experimental investigations with clear clinical relevance, original clinical studies and review articles.