MicroRNA‑93 inhibits inflammatory responses and cell apoptosis after cerebral ischemia reperfusion by targeting interleukin‑1 receptor‑associated kinase 4

The present study aimed to investigate changes in the expression of interleukin (IL)‑1 receptor‑associated kinase 4 (IRAK4) and microRNA (miRNA or miR)‑93 in mice with cerebral ischemia reperfusion (CIR) injury, as well as the association and regulatory mechanism between IRAK4 and miR‑93. The CIR mouse model was constructed and mouse microglia BV2 cells were transfected with miR‑93 mimic or miR‑93 inhibitor. Quantitative polymerase chain reaction was used to measure the expression of mRNA and miR‑93. Western blotting was performed to determine protein expression. Enzyme‑linked immunosorbent assays were performed to measure the concentrations pro‑inflammatory factors. The expression of miR‑93 in CIR mice brains was significantly reduced, while Ago‑miR‑93 (a type of miRNA analog) increased its expression. Ago‑miR‑93 alleviated neurological deficits and reduced cerebral infarction volume in the mice. Furthermore, Ago‑miR‑93 inhibited inflammatory responses following CIR. Ago‑miR‑93 decreased the rate of cell apoptosis following CIR. In addition, miR‑93 downregulated IRAK4 protein expression, but did not alter its mRNA expression levels in BV2 cells. miR‑93 expression reduced the expression of pro‑inflammatory factors in BV2 cells. Ago‑miR‑93 inhibited IRAK4 expression in the brain tissues of CIR mice. The present study demonstrated that miR‑93 inhibits inflammatory responses and cell apoptosis following CIR by targeting the IRAK4 signaling pathway.