LncRNA NR024118 is downregulated in sepsis and inhibits LPS‑induced apoptosis of cardiomyocytes
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- Published online on: April 8, 2021 https://doi.org/10.3892/mmr.2021.12073
- Article Number: 434
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Copyright: © Qin et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 4.0].
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Abstract
It has been reported that lncRNA‑NR024118 can suppress lipopolysaccharide (LPS)‑induced inflammatory responses, which promote sepsis. The present study aimed to investigate the involvement of NR024118 in sepsis. Research subjects included 82 patients with sepsis without myocardial dysfunction (MD), 35 patients with sepsis with MD and 82 healthy controls. The expression levels of NR024118 in plasma collected from these participants and LPS‑induced AC16 cells were measured by reverse transcription‑quantitative PCR. The expression levels of IL‑16 in these plasma samples and LPS‑induced AC16 cells were measured by ELISA. The correlation between the expression levels of NR024118 and IL‑6 across plasma samples were analyzed by Pearson's correlation coefficient. The action potential duration (APD) was measured at 50 and 90% repolarization. Cell apoptosis was determined by cell apoptosis assay. The expression levels of p‑transcription factor p65 were detected by western blot analysis. NF‑κB activity were analyzed by luciferase reporter assay. It was found that NR024118 was downregulated and IL‑6 was upregulated in the plasma of patients with sepsis. Among patients with sepsis, the individuals with MD exhibited even lower expression levels of NR024118 and higher expression levels of IL‑6. Among patients with sepsis with MD, the expression levels of NR024118 and IL‑6 were inversely correlated. LPS could induce MD to construct the sepsis models based on the increased expression levels of TNF‑α, IL‑1β, IL‑6 and shortened APD by LPS‑mediated induction. Overexpression of NR024118 significantly reduced the secretion of IL‑6 and apoptosis of cardiomyocytes under LPS treatment. Functional studies demonstrated that NR024118 had negative regulation on p65 phosphorylation and NF‑κB activation. NR024118 was suppressed in sepsis and inhibited LPS‑induced apoptosis of cardiomyocytes.
