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

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).