依达拉奉对脓毒血症大鼠急性肺损伤的保护机制研究

目的：探讨依达拉奉对脓毒血症致急性肺损伤（ALI）的保护机制。方法将60只雄性SD大鼠随机分3组：对照组（NS组）、模型组（LPS组）及依达拉奉治疗组（ED组），每组20只。LPS和ED组采用尾静脉注射LPS（10mg·kg-1）建立ALI模型，ED组随后立即尾静脉注射依达拉奉（5mg·kg-1）。LPS注射6h后抽取动脉血行血气分析测氧分压（PaO2）、二氧化碳分压（PaCO2）、氧合指数（PaO2/FiO2），提取肺组织测定干/湿重比值（D/W），观察肺组织病理改变，测定血浆中肿瘤坏死因子-α（TNF-α）、白细胞介素6（IL-6）含量。结果与NS组比较，LPS组肺组织D/W、动脉血气测得PaO2、PaCO2、PaO2/FiO2显著下降，肺损伤病理评分及血浆TNF-α、IL-6升高（P＜0．05）。与LPS比较，ED组肺组织D/W、动脉血气测得PaO2、PaCO2、PaO2/FiO2升高，肺损伤病理评分及血浆TNF-α、IL-6明显下降（P＜0.05），但仍高于NS组（P＜0．05）。结论依达拉奉对急性肺损伤具有保护作用，其机制可能是通过清除肺内氧自由基，减少炎性细胞因子TNF-α、IL-6产生。

Mechanisms of Protective Effects of Edaravone on Acute Lung Injury in Rats with Sepsis

Objective To explore the mechanisms of protective effects of edaravone on sepsis-induced acute lung injury（ALI）.Methods Sixty healthy male SD rats were randomly divided into three groups：control group（NS group,n=20）,model group（LPS group,n=20）and edaravone treatment group（ED group,n=20）.ALI was induced by tail vein injection of LPS（10 mg·kg-1 ） in LPS group and ED group.In addition,ED group was given tail vein injection of edaravone（5 mg· kg-1 ）.The arterial blood and lung tissue samples were collected at 6 hours after LPS injection. The oxygen partial pressure（PaO2 ）,carbon dioxide partial pressure（PaCO2 ）and oxygenation in-dex（PaO2/FiO2 ）were measured and the wet/dry（W/D）weight ratio of lung tissue was deter-mined.Furthermore,pathological changes in lung tissue were observed and tumor necrosis factor （TNF-α）and interleukin-6 （IL-6）levels in plasma were detected.Results Compared with NS group,W/D lung weight ratio,PaO2 ,PaCO2 and PaO2/FiO2 decreased in LPS group（P 〈0.05）, and pathological scores and plasma TNF-α and IL-6 levels increased in both LPS group and NS group（P 〈0.05）.Compared with LPS group,W/D lung weight ratio,PaO2 ,PaCO2 and PaO2/FiO2 increased and pathological scores and plasma TNF-αand IL-6 levels decreased in LPS group （P 〈0.05）.Conclusion Edaravone exerts protective effects on ALI,and the mechanisms of ac-tion may be mediated by scavenging free radicals and reducing the production of TNF-a and IL-6.