MiR-208a reduces inflammatory responses in heart failure rats through β-catenin pathway

Abstract

Purpose: To investigate the effect of micro-ribonucleic acid (miR)-208a on heart failure (HF) in rats through β-catenin pathway.Methods: A total of 24 specific pathogen-free female Sprague-Dawley rats were enrolled and randomly divided into 3 equal groups, namely, control (normal group), model, and study group (miR-208a), with 8 rats each. Echocardiography was utilized to evaluate cardiac function, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was applied to examine cardiomyocyte apoptosis. Finally, expression levels of interleukin (IL)-6 and IL-10 were determined using enzymelinked immunosorbent assay (ELISA). Expression of matrix metalloproteinases (MMPs) was determined via immunohistochemistry assay, while western blotting was used to measure expression of β-catenin.Results: The mRNA expression level of miR-208a was significantly lower in model group than control and study group (p < 0.05). Cardiac function of rats in model group was significantly better than other groups (p < 0.05). Cardiomyocyte apoptosis was significantly increased in model group than in other groups (p < 0.05). Furthermore, expression levels of MMPs, IL-6 and IL-10 in model group were elevated in comparison with those in study and control groups (p < 0.05).Conclusion: MiR-208a reduces inflammatory response and deposition of extracellular matrix in rats with HF through inhibition of β-catenin signaling pathway, thereby restoring cardiac function.