MicroRNA‑23a‑3p targeting of HMGB1 inhibits LPS‑induced inflammation in murine macrophages in vitro
- Qi Sun
- Bing Wang
- Mengqiu Li
Affiliations: Department of Critical Care Medicine, The Jingzhou Central Hospital of Hubei, Jingzhou, Hubei 434000, P.R. China
- Published online on: March 10, 2022 https://doi.org/10.3892/etm.2022.11251
Copyright: © Sun
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Inflammatory cytokines, including high mobility group box 1 (HMGB1), play a key role in sepsis via various mechanisms, some of which remain unknown. Sepsis is a common cause of death in patients admitted to the intensive care unit. MicroRNAs (miRs) serve an important role in the inflammatory response. The present study aimed to investigate the role of miR‑23a‑3p in macrophage inflammation and the targeted regulation of HMGB1 expression. The murine macrophage cell line RAW264.7 was subjected to lipopolysaccharide (LPS) treatment to mimic the inflammation involved in sepsis in vitro. Reverse transcription‑quantitative PCR was performed to measure miR‑23a‑3p expression and mRNA expression. Protein levels were determined using ELISA and western blotting. The target binding relationship between miR‑23a‑3p and the HMGB1 3'untranslated region was predicted and validated with a dual luciferase reporter assay. HMGB1 expression was increased and miR‑23a‑3p expression significantly reduced in patients with sepsis and in LPS‑treated RAW264.7 cells in comparison with controls. Overexpression of miR‑23a‑3p reduced interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α expression in RAW264.7 cells under LPS stimulation, while silencing of miR‑23a‑3p elevated the expression of IL‑6 and TNF‑α in comparison with controls. The inhibitory effect of miR‑23a‑3p on LPS‑induced inflammation could be abolished by HMGB1 upregulation in RAW264.7 cells. HMGB1 was targeted by miR‑23a‑3p. miR‑23a‑3p is expressed at reduced levels during inflammation in sepsis, and overexpression of miR‑23a‑3p inhibits LPS‑induced inflammation in murine macrophages in vitro by directly downregulating HMGB1. The results of the present study provided a novel insight into the molecular mechanism underlying HMGB1 expression at the post‑transcriptional level in sepsis.