title: Monoammonium glycyrrhizinate inhibited the inflammation of LPS-induced acute lung injury in mice.
abstract: Monoammonium glycyrrhizinate (MAG) was the aglycone of glycyrrhizin derived from licorice. In this study, the anti-inflammatory effects of MAG on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the possible mechanisms involved in this protection were investigated. Pretreatment with MAG prior to the administration of intratracheal LPS significantly induced a decrease in lung wet weight/dry weight ratio, in total leukocyte number and neutrophil percent in the BALF, and in myeloperoxidase (MPO) activity of lung in dose-dependent manners. At the same time, pretreatment with MAG also significantly improved the super oxide dismutase (SOD) activity and induced the malondialdehyde (MDA) content in the bronchoalveolar lavage fluid (BALF). Importantly, pretreatment with MAG prevented an increase in cyclic adenosine monophosphate-phosphodiesterase (cAMP-PDE) activity of lung in a dose-dependent manner. In addition, it can up-regulate the interleukin-10 (IL-10) level and down-regulate the tumor neurosis factor-α (TNF-α) level in the lung tissue of ALI mice. These results showed that anti-inflammatory effects of MAG against the LPS-induced ALI may be due to its ability of primary inhibition of cAMP-PDE activity, oxidative stress and its regulation of cytokine effects. Thus the results support that use of MAG is beneficial in the treatment of ALI and ARDS.
authors.affiliation: Zhejiang Key Laboratory for Diagnosis and Therapy of National Disease, Department of Laboratory, Children's Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
authors.forename: Jian-Rong
authors.initials: JR
authors.lastname: Shi
authors.forename: Lian-Gen
authors.initials: LG
authors.lastname: Mao
authors.forename: Ruo-An
authors.initials: RA
authors.lastname: Jiang
authors.forename: Yun
authors.initials: Y
authors.lastname: Qian
authors.forename: Hui-Fang
authors.initials: HF
authors.lastname: Tang
authors.forename: Ji-Qiang
authors.initials: JQ
authors.lastname: Chen
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D002199:Capillary Permeability / Q000187:drug effects; D000242:Cyclic AMP / Q000378:metabolism; D019695:Glycyrrhizic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy*; D016753:Interleukin-10 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008171:Lung Diseases / Q000139:chemically induced*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology; D010084:Oxidation-Reduction; D009195:Peroxidase / Q000378:metabolism; D010727:Phosphoric Diester Hydrolases / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D008315:Malondialdehyde; D019695:Glycyrrhizic Acid; D000242:Cyclic AMP; D009195:Peroxidase; D013482:Superoxide Dismutase; D010727:Phosphoric Diester Hydrolases