miR‑351‑5p aggravates lipopolysaccharide‑induced acute lung injury via inhibiting AMPK.

Inflammation and oxidative stress have indispensable roles in the development of acute lung injury (ALI). MicroRNA (miRNA/miR)‑351‑5p was initially identified as a myogenesis‑associated miRNA; however, its role in lipopolysaccharide (LPS)‑induced ALI remains unclear. The aim of the present study was to investigate the role and potential mechanisms of miR‑351‑5p in ALI. ALI was induced through a single intratracheal injection of LPS for 12 h, and miR‑351‑5p agomir, antagomir or their corresponding negative controls were injected into the tail vein before LPS stimulation. Compound C, 2',5'‑dideoxyadenosine and H89 were used to inhibit AMP‑activated protein kinase (AMPK), adenylate cyclase and protein kinase A (PKA), respectively. miR‑351‑5p levels in the lungs were significantly increased in response to LPS injection. miR‑351‑5p antagomir alleviated, while miR‑351‑5p agomir aggravated LPS‑induced oxidative stress and inflammation in the lungs. The present results also demonstrated that miR‑351‑5p antagomir attenuated LPS‑induced ALI via activating AMPK, and that the cAMP/PKA axis was required for the activation of AMPK by the miR‑351‑5p antagomir. In conclusion, the present study indicated that miR‑351‑5p aggravated LPS‑induced ALI via inhibiting AMPK, suggesting that targeting miR‑351‑5p may help to develop efficient therapeutic approaches for treating ALI.