Overexpression of microRNA-590-3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF-κB signaling pathway by binding to RIPK1.

Ischemic heart disease is widely considered as a major health threat, which causes a high number of deaths every year worldwide. Much evidence has shown that oxidative stress (OS) is implicated in the pathogenesis of ischemia-reperfusion injury (IRI). This study aims to evaluate the effect of miR-590-3p on the OS of IRI mice through the nuclear factor kappa-B (NF-κB) signaling pathway by targeting receptor-interacting protein kinase 1 (RIPK1). IRI mouse models were established for extracting myocardial tissues and isolating myocardial cells. The expression of inflammatory related-factors was detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD) and malondialdehyde (MDA) in tissues were determined. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were performed to assess the role of miR-590-3p in the expression of NF-κB-related factors and apoptosis-related factors. Besides, the regulatory effects of miR-590-3p on myocardial cell proliferation and apoptosis were also assessed. According to the obtained results, we found that IRI mice displayed higher expression of tumor necrosis factor-α, interleukin (IL)-6, and interferon-γ, lower expression of IL-10 in serum, a decreased SOD level, and an increased MDA level. In addition, RIPK1 was determined as a target gene of miR-590-3p. After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found. Our study demonstrates that miR-590-3p can alleviate the OS of IRI mice through the inhibition of the RIPK1 and NF-κB signaling pathway. Thus, miR-590-3p represents a potential target for IRI repair.