Abstract
BackgroundInflammation plays an important role in the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The long non-coding RNA (lncRNA) MINCR is closely related to inflammation injury. This study was performed to explore the protective effects and mechanisms of MINCR in lipopolysaccharide (LPS)-induced lung injury and inflammation.MethodsThe expression levels of MINCR and miR-146b-5p in lung tissue status were detected by using quantitative real-time polymerase chain reaction (qRT-PCR), hematoxylin and eosin staining, immunohistochemical staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Enzyme-linked immunosorbent assay and Western blotting analysis were used to detect the expression of inflammatory factors such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 in lung tissue. The relationship between MINCR, miR-146b-5p, and TRAF6 was explored using bioinformatics analysis and luciferase assay.ResultsThe expression levels of MINCR were increased in a mouse model of LPS-induced ALI and small airway epithelial cells (SAECs). shMINCR resulted in increased cell viability and decreased apoptosis, which protected against LPS-induced cell damage. shMINCR can inhibit the formation of neutrophil extracellular traps, neutrophil numbers, myeloperoxidase activity, and the production of inflammatory cytokines IL-6, IL-1β, and TNF-α induced by LPS. The silencing of miR-146b-5p reversed the effects of MINCR on LPS-induced lung damage. Sh-MINCR decreased the expression levels of TRAF6 and p-P65 in LPS-induced SAECs and lung tissues. Co-transfection of sh-MINCR with miR-146b-5p inhibitor reversed the effect of sh-MINCR on the expression of TRAF6 and p-P65.ConclusionsMINCR may induce alveolar epithelial cell injury and inflammation and aggravate the progression of ALI/ARDS through miR-146b-5p and TRAF6/NF-κB pathways, which would provide a promising target for the treatment of ALI/ARDS.
Highlights
Inflammation plays an important role in the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)
MINCR was upregulated in ALI mouse model and LPS‐injured alveolar epithelial cells Compared to the control group, the expression levels of MINCR in the lung tissue of LPS-injured mice were significantly increased (P < 0.05, Fig. 1A)
small airway epithelial cells (SAECs) were exposed to LPS to simulate ALI in vitro, and the expression levels of MINCR gradually increased with an increase in the duration of LPS and an increase in the concentration of the effect (P < 0.05, Fig. 1B and C)
Summary
Inflammation plays an important role in the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This study was performed to explore the protective effects and mechanisms of MINCR in lipopolysaccharide (LPS)induced lung injury and inflammation. Acute lung injury (ALI) is a disease that is widely distributed worldwide. It is an acute progressive insufficiency or respiratory failure caused by various internal and external factors of the lung, with a mortality rate of up to 40% (Tao et al 2019). It is important to elucidate the regulatory mechanisms and signaling pathways involved in the pathological process of ALI to provide targeted drugs for clinical treatment
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