miR‑186‑5p regulates the inflammatory response of chronic obstructive pulmonary disorder by targeting HIF‑1α.

Chronic obstructive pulmonary disorder (COPD) is a chronic respiratory disease that is a major cause of morbidity and mortality worldwide. Previous studies have shown that miR-186-5p expression is significantly increased in COPD and is involved in multiple physiological and pathological processes. However, the role of miRNA-186-5p in the inflammatory response of COPD remains unclear. In this study, an in vitro model of COPD was established using lipopolysaccharide (LPS)-induced human bronchial epithelial cells (BEAS-2B). CCK-8 assays, flow cytometry, and a Muse cell analyzer were used to determine cell viability, cell cycle distribution, and apoptosis, respectively. The production of TNF-α and IL-6 were measured by ELISA. Reverse-transcription-quantitative PCR and western blotting were used to analyze mRNA and protein expression levels. The targeting relation between miR-186-5p and HIF-1α was discovered using dual-luciferase reporter assays. The results showed that transfection of miR-186-5p inhibitor inhibited cell proliferation and promoted cell apoptosis in the LPS-induced BEAS-2B cells. Inhibition of miR-186-5p markedly increased the levels of TNF-α and IL-6. miR-186-5p directly targeted and negatively regulated HIF-1α expression. In addition, inhibition of miR-186-5p increased the expression of the NF-κB pathway protein p-p65. In conclusion, it was found that inhibiting miR-186-5p may improve inflammation of COPD through HIF-1α in LPS-induced BEAS-2B cells, possibly by regulating NF-κB signaling. These findings provide a novel potential avenue for the clinical management of COPD. Future research is required to determine the mechanism of the interaction between miR-186-5p and HIF-1α in COPD. [ABSTRACT FROM AUTHOR]