Lipoxin A4 attenuates LPS-induced acute lung injury via activation of the ACE2-Ang-(1-7)-Mas axis:

摘要: Previous studies have reported that lipoxin A4 (LXA4) and the angiotensin I-converting enzyme 2 (ACE2), angiotensin-(1-7) [Ang-(1-7)], its receptor Mas [ACE2-Ang-(1-7)-Mas] axis play important protective roles in acute lung injury (ALI). However, there is still no direct evidence of LXA4-mediated protection via ACE2-Ang-(1-7)-Mas during ALI. This work was performed using an LPS-induced ALI mouse model data indicated following. First, animal established successfully LXA4 ameliorated Second, could increase concentration activity ACE2 levels Ang-(1-7) markedly. Third, decreased TNF-α, IL-1β, reactive oxygen species while increasing IL-10 levels. Fourth, inhibited activation NF-κB signal pathway repressed degradation inhibitor NF-κB, phosphorylation translocation NF-κB. Finally, more importantly, BOC-2 (LXA4 inhibitor), MLN-4760 (ACE2 A779 (Mas antagonist) were found to reverse all effects LXA4. Our provide protects from through regulation axis.