Anti-Inflammatory Effects of Monoammonium Glycyrrhizinate on Lipopolysaccharide-Induced Acute Lung Injury in Mice through Regulating Nuclear Factor-Kappa B Signaling Pathway. (18th March 2015)

• Record Type: Journal Article
• Authors: Huang, Xiaoying; Tang, Jiangfeng; Cai, Hui; Pan, Yi; He, Yicheng; Dai, Caijun; Chen, Ali; Yu, Xiaoming; Chen, Mayun; Zou, Lizhen; Wang, Liangxing
• Other Names: Kim Cheorl-Ho Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2015(2015)
• Publication Date: 2015-03-18
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2015/272474
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : 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-1 β (IL-1 β ) in the BALF were measured by ELISA. The activation of NF- κ B p65 and I κ B- 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-1 β in BALF. Furthermore, we demonstrated that MAG suppressed activation of NF- κ B 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- κ B signaling pathway. Monoammonium glycyrrhizinate may be a potential therapeutic reagent for ALI.