中文摘要：

目的探究吴茱萸碱（evodiamine,EVO）对酵母多糖（zymosan）诱导的急性肺损伤的保护效应及其作用机制。方法 24只6-8周龄雄性C57BL/6小鼠,按随机数字表法分为正常对照组、EVO对照组、模型组、EVO治疗组,每组6只。各组分别于处理作用12 h后处死小鼠,收集眼眶血及肺组织。酶联免疫吸附法（ELISA）检测血液及肺组织中白介素-6（interleukin-6,IL-6）、肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）水平及肺组织髓过氧化物酶（myeloperoxidase,MPO）活性及核转录因子NF-κB p65的DNA结合活性,TUNEL法检测肺组织细胞凋亡情况,HE染色观察肺组织病理改变并测量肺湿干质量比。结果酵母多糖作用12 h后,小鼠出现精神萎靡、活动减少等症状。EVO治疗组小鼠状态有所好转。EVO可明显改善酵母多糖所致的肺泡壁毛细血管扩张充血及炎性细胞浸润,降低肺湿干质量比,并显著下调酵母多糖刺激下血清和肺脏中IL-6和TNF-α的含量（P〈0.01）,同时抑制肺组织中MPO含量以及NF-κB p65的DNA结合活性（P〈0.01）。结论 EVO可缓解酵母多糖诱导的急性肺损伤。该作用可能是通过抑制NF-κB的活性以减少炎症介质释放实现。

英文摘要：

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 C57 BL /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 Td T-mediated d UTP 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（ P〈0. 01）. EVO also attenuated the MPO activity and DNA-binding activity of NF-κB p65 in the lung tissue of mice after ZYM treatment（ P〈0. 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.