Deregulated miR-146a-3p alleviates disease progression in atherosclerosis through inactivating NF-κB: An experimental study

Background:Atherosclerosis (AS), as a complex chronic inflammatory disease, is 1 of the main causes of cardiovascular and cerebrovascular diseases. This study aimed to confirm the direct interaction between miR-146a-3p and NF-kappa B, and explore the role of miR-146a-3p/NF-kappa B in the regulation of inflammation in AS.Methods:Bioinformatic prediction and dual-luciferase reporter assay were used to confirm the interaction between miR-146a-3p and NF-kappa B. Lipopolysaccharides stimulation was performed to establish AS inflammatory cell model, and the levels of pro-inflammatory cytokines were estimated using an enzyme-linked immunosorbent assay. miR-146a-3p and NF-kappa B expression were evaluated using reverse transcription quantitative PCR, and their clinical value was examined using a receiver operating characteristic curve.Results:Inflammatory cell model showed increased IL-1 beta, IL-6, and TNF-alpha. NF-kappa B was a target gene of miR-146a-3p, and mediated the inhibitory effects of miR-146a-3p on inflammatory responses in the cell model. In patients with AS, miR-146a-3p/NF-kappa B was associated with patients' clinical data and inflammatory cytokine levels, and aberrant miR-146a-3p and NF-kappa B showed diagnostic accuracy to distinguish AS patients from healthy populations.Conclusion:miR-146a-3p might inhibit inflammation by targeting NF-kappa B in AS progression, and miR-146a-3p/ NF-kappa B might provide novel biomarkers and therapeutic targets for the prevention of AS and related vascular events.