Objective      To determine the protective effect of evodiamine (EVO) in ameliorating sepsis-associated acute lung injury (ALI) induced by zymosan (ZYM) injection and investigate the underlying mechanism. Methods      Twenty-four male C57BL/6 mice were randomly divided into 4 groups

that is

control group

EVO control group

model group and EVO treatment group (n=6 for each group). In 12 h after drug administration

all mice were sacrificed to collect blood samples and lung tissue samples. The concentrations of interleukin-6 (IL-6) and tumor necrosis factorα (TNF-α) in the plasma and lung tissue

as well as the activity of myeloperoxidase (MPO) and DNA-binding activity of nuclear factor-κB p65 (NF-κB p65) in the lung tissue were detected by enzyme linked immunosorbent assay (ELISA). Cell apoptosis in lung tissue was determined by TdT-mediated dUTP nick end labeling (TUNEL)

and the pathological changes of lung tissue cells were observed after HE staining. Lung wet/dry ratio was also calculated. Results     In 12 h after ZYM injection

the mice showed mental fatigue and reduced activity. EVO treatment improved the general status of the mice

and reduced the concentrations of TNF-α and IL-6 in the serum and lung tissue (P0.01). EVO also attenuated the MPO activity and DNA-binding activity of NF-κB p65 in the lung tissue of mice after ZYM treatment (P0.01). Besides that

histological examination demonstrated that ZYM-treated mice had severe inflammatory responses in lung tissues (such as hyperemia

edema and neurophils infiltration)

but EVO treatment significantly ameliorated these pathological changes. Conclusion       EVO can reduce sepsis-associated acute lung injury in the mice

which may be achieved via suppressing DNA-binding activity of NF-κB p65 and reduction of synthesis and release of cytokines.