miRNA-302e attenuates inflammation in infantile pneumonia though the RelA/BRD4/NF-κB signaling pathway.

In the present study, the main focus was investigating the role of microRNA (miRNA)‑302e in infantile pneumonia (IP) and exploring the potential protective mechanisms. Briefly, the expression of miRNA‑302e was reduced in a mouse model of IP. In addition, the administration of anti‑miRNA‑302e increased inflammation and induced the protein expression of RelA, bromodomain‑containing protein 4 (BRD4) and nuclear factor (NF)‑κB in the in vitro model of IP. In contrast, over‑expression of miRNA‑302e reduced inflammation and suppressed the protein expression of RelA, BRD4 and NF‑κB in an in vitro model of IP. Small interfering (si)‑RelA attenuated the effects of miRNA‑302e on inflammation in an in vitro model of IP. Consistently, si‑BRD4 or si‑NF‑κB attenuated the effects of miRNA‑302e on inflammation in an in vitro model of IP. Taken together, the results of the present study demonstrated that miRNA‑302e attenuated inflammation in IP through the RelA/ BRD4/ NF‑κB signaling pathway.