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目的 探讨基因Abro1在脂多糖(LPS)诱导的急性肺损伤中的作用.方法 Abro1基因敲除型(KO)小鼠和野生型(WT)C57BL/6小鼠各14只,随机各等分为两组,分别采用肺部气溶胶给药系统给予LPS(10 mg/kg)或等体积生理盐水预处理,给药6 h和24 h后收集样本.应用HE染色观察肺组织病理改变;比较各组支气管肺泡灌洗液中的细胞数目和肺组织中髓过氧化物酶(MPO)含量,检测支气管肺泡灌洗液中IL-6水平以及肺组织mRNA水平.结果 给药24 h后,与肺部接受生理盐水相比,LPS处理组小鼠肺组织显著损伤,主要表现为炎性细胞浸润,肺泡壁增厚,但Abro1 KO小鼠的肺组织病理损伤程度显著低于WT小鼠;LPS处理6 h后,KO小鼠支气管肺泡灌洗液中募集的炎性细胞数目和肺组织MPO含量显著低于WT小鼠(P<0.05),而其IL-6水平及肺组织mRNA水平均低于WT小鼠(P<0.05).结论 敲除Abro1可减轻LPS诱导的肺部炎症反应,减轻肺损伤.“,”Objective To investigate the effect of Abro1 on acute respiratory distress syndrome(ARDS)/acute lung injury(ALI)in mice.Methods Abro1 knock-out(KO)mice and wild type(WT)mice were both randomly divided into two groups for intratracheal instillation of lipopolysaccharide(LPS)or normal saline.At 6 or 24 hours after treatment, the pathological changes in lung tissue were observed by HE staining.At 6 hours after treatment,inflammatory immune cells and cytokines production(IL-6)in the bronchoalveolar lavage fluid were examined.Myeloperoxidase(MPO)and the mRNA level of IL-6 in the lung tissue were compared.Results At 24 hours after treatment, compared with WT mice treated with LPS,Abro1 KO mice showed a significantly lower lung injury score.At 6 hours after treatment,Abro1 depletion resulted in reduced levels of inflammatory immune cell infiltration and cytokines production(IL-6)in the bronchoalveolar lavage fluid(P<0.05).In addition,the MPO content and the mRNA level of IL-6 in the lung tissue were much lower than those in WT mice treated with LPS for 6 hours(P<0.05).Conclusion Abro1 deficiency can attenuate LPS-induced ARDS/ALI.