• Xiaoying Huang, Jiangfeng Tang, Hui Cai, Yi Pan, Yicheng He, Caijun Dai, Ali Chen, Xiaoming Yu, Mayun Chen, Lizhen Zou, and Liangxing Wang.
• Department of Respiratory, The First Affiliated Hospital of Wenzhou Medical University and Key Laboratory of Heart and Lung, Wenzhou, No. 2 Fu Xue Lane, Lucheng District, Wenzhou, Zhejiang 325035, China.
• Evid Based Compl Alt. 2015 Jan 1; 2015: 272474.

AbstractThe 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.

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