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作 者:张秋金[1] 沈洪[1] 张维[1] 李银平[2] 黎檀实[1]
机构地区:[1]解放军总医院急诊科,北京100853 [2]天津市天和医院
出 处:《中国危重病急救医学》2005年第6期370-372,i002,共4页Chinese Critical Care Medicine
基 金:解放军总后"十五"指令性课题(04LX043)
摘 要:目的探讨联合应用甲基泼尼松龙和纳洛酮对内毒素(LPS)所致急性肺损伤(ALI)大鼠肺组织核转录因子κB(NFκB)表达的作用。方法建立大鼠LPS吸入性ALI模型(LPS3mg/kg气管内注射)。85只大鼠随机分为5组:生理盐水对照组,LPS损伤组,甲基泼尼松龙组(LPS+甲基泼尼松龙),纳洛酮组(LPS+纳洛酮),联合用药组(LPS+甲基泼尼松龙+纳洛酮)。采用放射免疫法检测大鼠血清白细胞介素8(IL8)水平,并应用免疫组化法观察肺组织NF-κBp65蛋白表达的变化。结果经气道吸入LPS可致大鼠发生ALI。ALI大鼠肺组织NFκBp65蛋白表达明显升高(P<0.05或P<0.01),IL-8水平亦明显增高(P<0.05或P<0.01),单用甲基泼尼松龙或纳洛酮组肺组织NF-κBp65蛋白表达率及IL-8水平均较LPS损伤组明显降低,以联合用药组更为明显(P<0.05或P<0.01)。结论联合应用甲基泼尼松龙和纳洛酮可降低LPS吸入性ALI大鼠血清IL-8升高,并显著抑制肺组织NF-κBp65蛋白表达。Objective To investigate the effects of a combination of naloxone and methylprednisolone on nuclear factorκB (NFκB) p65 expression in the lung tissue in lipopolysaccharide (LPS) induced acute lung injury(ALI) in rats. Methods ALI models were reproduced by intratracheal instillation of LPS ( 3 mg/kg ). Four hours after LPS instillation, rats were randomly divided into five groups: normal saline group, LPS group, methylprednisolone group, naloxone group (LPS+naloxone) and combined drug group (LPS+naloxone+ methylprednisolone). The level of interleukin8 (IL8) in serum was measured by immunoassay . Meanwhile, the expression of NFκB p65 in the lung tissue was determined with immunohistochemicalstaining. Results Naloxone and methylprednisolone significantly reduced the LPSinducedincrease in IL8 concentrations in serum in vivo, and suppressed the activation of NFκB p65 in the lung tissue. Conclusion NFκB activation is involved in the LPSinduced ALI in rats. Combinationof naloxone and methylprednisolone could suppress the increase of IL8 content and NFκB activation in the lung tissue of rat in vivo in our experiment.
关 键 词:甲基泼尼松龙 大鼠肺组织 急性肺损伤 核转录因子-ΚB 纳洛酮 白细胞介素-8(IL-8) 联用 0.05 IL-8水平 血清IL-8 气管内注射 LPS 免疫法检测 免疫组化法 蛋白表达率 ALI 方法建立 生理盐水 大鼠血清 吸入性 联合用 NF
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