Apelin-13-Mediated AMPK ameliorates endothelial barrier dysfunction in acute lung injury mice via improvement of mitochondrial function and autophagy

Maintaining the pulmonary endothelial barrier that prevents the exudation of inflammatory factors and proteins is the key to the treatment of acute lung injury (ALI). Apelin-13 plays an important role in vascular diseases; however, the protective effects of Apelin-13 on ALI with pulmonary endothelial barrier are unknown. Therefore, mice and human umbilical vein endothelial cells (HUVECs) were injured by LPS following Apelin-13 administration. ALI mice showed reduced pulmonary vascular permeability, adhesion junction, mitochondrial function, mitochondrial biogenesis, and autophagy compared to the control group. Apelin-13 administration in ALI mice ameliorated LPS-induced lung injury, pulmonary vascular permeability, mitochondrial function, and promoted autophagic flux in mice and HUVECs. However, the effect of Apelin-13 was reduced after AMPK inhibition using Compound C. These data suggest that Apelin-13 ameliorates pulmonary vascular permeability in mice with ALI induced by LPS, which may be related to enhanced phosphorylation of AMPK to regulate mitochondrial function and autophagy.

Automated summary

Apelin-13 administration ameliorates pulmonary vascular permeability and mitochondrial function, and promotes autophagic flux in mice and HUVECs with ALI induced by LPS. The protective effects of Apelin-13 were found to be related to enhanced phosphorylation of AMPK to regulate mitochondrial function and autophagy, but this effect was reduced after AMPK inhibition.