Anti-Inflammatory Effects of Monoammonium Glycyrrhizinate on Lipopolysaccharide-Induced Acute Lung Injury in Mice through Regulating Nuclear Factor-Kappa B Signaling Pathway

Abstract EN

The present study aimed to investigate the therapeutic effect of monoammonium glycyrrhizinate (MAG) on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice and possible mechanism.

Acute lung injury was induced in BALB/c mice by intratracheal instillation of LPS, and MAG was injected intraperitoneally 1 h prior to LPS administration.

After ALI, the histopathology of lungs, lung wet/dry weight ratio, protein concentration, and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined.

The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the BALF were measured by ELISA.

The activation of NF-κB p65 and IκB-α of lung homogenate was detected by Western blot.

Pretreatment with MAG attenuated lung histopathological damage induced by LPS and decreased lung wet/dry weight ratio and the concentrations of protein in BALF.

At the same time, MAG reduced the number of inflammatory cells in lung and inhibited the production of TNF-α and IL-1β in BALF.

Furthermore, we demonstrated that MAG suppressed activation of NF-κB signaling pathway induced by LPS in lung.

The results suggested that the therapeutic mechanism of MAG on ALI may be attributed to the inhibition of NF-κB signaling pathway.

Monoammonium glycyrrhizinate may be a potential therapeutic reagent for ALI.