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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.

experimental and therapeutic medicine

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