首页> 中文期刊> 《南昌大学学报(医学版)》 >依达拉奉对脓毒血症大鼠急性肺损伤的保护机制研究

依达拉奉对脓毒血症大鼠急性肺损伤的保护机制研究

         

摘要

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 (10 mg·kg-1)建立 ALI 模型,ED 组随后立即尾静脉注射依达拉奉(5 mg·kg-1)。LPS 注射6 h 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。%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.

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