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机构地区:[1]第四军医大学唐都医院呼吸内科,西安710032
出 处:《中华肺部疾病杂志(电子版)》2014年第5期30-33,共4页Chinese Journal of Lung Diseases(Electronic Edition)
基 金:国家自然科学基金面上项目(81270124)
摘 要:目的探讨海水吸入型肺损伤大鼠肺组织中核因子-κB(NF-κB)通路的变化以及1,25-二羟维生素D3对其干预作用。方法 32只大鼠完全随机分为空白对照组、海水处理组、VitD3预处理组和地塞米松处理组,每组8只。采用气管内滴注海水(3 ml/kg)的方法制作海水吸入型急性肺损伤大鼠模型,观察肺部病理变化,用ELISA法检测肺组织中肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)的含量,Western blot检测磷酸化NF-κB的表达变化,免疫荧光观察A549细胞NF-κB核转移情况。结果海水吸入4 h后,大鼠肺部损伤明显,TNF-α和IL-1β的含量增高,NF-κB磷酸化以及核转移增多;1,25-二羟维生素D3预处理显著减轻了海水吸入导致的急性肺损伤,减少了炎症因子的释放,并且抑制了NF-κB磷酸化以及核转移。结论 NF-κB通路参与了海水吸入型肺损伤的发生发展,1,25-二羟维生素D3能够通过抑制NF-κB信号通路减轻肺损伤。Objective To observe the change of NF-κB pathway in seawater aspiration-induced acute lung injury and the intervention effect of 1,25-(OH) 2VitD3.Methods A total of 32 rats were randomly divided into 4 groups:normal control group,seawater group,VitD3 pre-treated group and dexamethasone pretreated group.Every group contains 8 rats.Seawater aspiration-induced acute lung injury model was made by seawater instillation (3 ml/kg) into the airway.Pathology detection was carried out after modeling.The contents of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured by ELISA and the expression of phospho-NF-κB was measured by western blot.Immunofluorescence was used to detect the nuclear translocation of NF-κB in A549 cells.Results After 4 h seawater stimulation,lung injury was obvious and the contents of TNF-α and IL-1β were increased.The expression of phospho-NF-κB was up-regulated and nuclear translocation was enhanced.However,pre-treatment of 1,25-(OH) 2 VitD3 attenuated lung injury,suppressed the release of pro-inflammation cytokines,and inhibited the expression of phospho-NF-κB and the nuclear translocation.Conclusion NF-κB pathway plays an important part in the seawater aspiration-induced acute lung injury and 1,25-(OH) 2VitD3 attenuated lung injury by inhibiting NF-κB pathway.
关 键 词:急性肺损伤 海水 1 25-二羟维生素D3 核因子-ΚB
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