Abstract: Objective The present study aimed to explored the effects and mechanism of action of gambogic(GA) on lipopolysaccharide(LPS)-induced acute lung injury(ALI) in Kunming mice. Methods ALI model was established by the injection of lipopolysaccharide into the tail vein of mice(4mg/kg, iv). The mice were randomly divided into control group(control), model group(model), GA group(GA), and pretreatment with GA of ALI group(GA+LPS). After six hours, the wet/dry weight ratio (W/D) of the lung , myeloperoxidase (MPO) activity in lung tissue, levels of total proteins and number of white blood cells in bronchoalveolar lavage fluid (BALF) were determined. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured by the enzyme-linked immunosorbent assay methods. Results Compared with control group, the wet/dry weight ratio (W/D) of the lung , MPO activity in lung tissue, levels of total proteins and number of white blood cells in BALF of LPS group obviously increased, in addition the level of lung tissue TNF-α and IL-1β in LPS group were significantly higher(all P<0.01), while in GA pretreatment groups alleviated all the changes in ALI mice. Conclusions GA pre-treatment attenuated LPS-induced ALI, possibly by inhibiting inflammatory cytokines production so as to decrease the recruitment of neutrophils, reduce pulmonary edema.

Key words: Gambogic acid, lipopolysaccharide, acute lung injury, tumor necrosis factor-α, interleukin-1β