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Monoammonium glycyrrhizinate inhibited the inflammation of LPS-induced acute lung injury in mice
Authors:Jian-Rong Shi  Lian-Gen Mao  Ruo-An Jiang  Yun Qian  Hui-Fang Tang  Ji-Qiang Chen
Affiliation:1. Zhejiang Respiratory Drugs Research Laboratory of SFDA of China, School of Medicine, Zhejiang University, Hangzhou 310058, China;2. Zhejiang Key Laboratory for Diagnosis and Therapy of National Disease, Department of Laboratory, Children''s Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China;3. National Talent Training Base, School of Medicine, Zhejiang University, Hangzhou 310058, China
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.
Keywords:Monoammonium glycyrrhizinate   Lipopolysaccharide   Acute lung injury   TNF-α   IL-10   cAMP-PDE   MMP-12   SOD   MDA   MPO
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