Abstract
Reactive oxygen species (ROS) have been clinically shown to be relevant in the progression of various apoptosis‑associated heart diseases. Our previous study demonstrated that microRNA (miR)‑423‑5p is involved in congestive heart failure (CHF) through the direct targeting of O‑GlcNAc transferase and the induction of apoptosis in cardiomyocytes. However, the role of miR‑423‑5p during ROS‑induced apoptosis remains to be elucidated. In the present study, the expression of miR‑423‑5p in cardiomyocytes following exposure to H2O2 was determined using reverse transcription‑quantitative polymerase chain reaction analysis. In addition, the effects of silencing of miR‑423‑5p, by using an miR‑423‑5p‑mimic during H2O2 treatment, on cardiomyocyte apoptosis were detected using a terminal deoxynucleotidyl transferase‑deoxyuridine triphosphate nick‑end labeling assay. The expression levels of the direct target of miR‑423‑5p and associated downstream targets were also examined. The results demonstrated that H2O2 significantly induced the expression of miR‑423‑5p in cardiomyocytes, in a time‑ and concentration‑dependent manner. The silencing of miR‑423‑5p by transfection with the miR‑423‑5p‑mimic eliminated the H2O2‑induced cardiomyocyte apoptosis and decrease in viability. The expression levels of the downstream targets of miR423‑5p were also increased by H2O2, and were decreased following the silencing of miR‑423‑5p. Collectively, the results of the present study demonstrated that miR‑423‑5p mediated H2O2‑induced apoptosis in the cardiomyocytes. Silencing of miR‑423‑5p significantly protected the cardiomyocytes from H2O2‑induced apoptosis, and this may provide a novel therapeutic target for apoptosis‑associated heart diseases.