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作 者:杨泳[1] 郭欣[2] 俞志成[1] 马加庆[1] 刘星玲[2] 李丽莎[2] 肖高鹏[2] 刘晓萌 李鑫楠[2] 沈劲松 李艳华[2] 刘睿[2]
机构地区:[1]昆明医科大学医学机能实验中心,云南昆明650500 [2]云南省第一人民医院麻醉科,云南昆明650032
出 处:《南方医科大学学报》2017年第10期1345-1350,共6页Journal of Southern Medical University
基 金:云南省教育厅一般项目(2014C027Y);云南省科技厅-昆明医科大学联合专项(2014FB-098);云南省卫生科技计划项目(2014NS244)
摘 要:目的探讨胞质型磷脂酶A2(C-PLA2)与核因子κB(NF-κB)间相互作用关系,阐明单肺通气上调C-PLA2表达的作用机制。方法 48只健康日本大耳白兔随机均分为8组:对照组;溶剂预处理组;NF-κB抑制剂(PDTC)/溶剂预处理组;C-PLA2抑制剂(AACOCF3)/溶剂预处理组;单肺通气组;溶剂预处理+单肺通气组;NF-κB抑制剂(PDTC)/溶剂预处理+单肺通气组和CPLA2抑制剂(AACOCF3)/溶剂预处理+单肺通气组。Western-blot和定量PCR分别用于检测肺组织C-PLA2和NF-κB蛋白及m RNA表达水平;ELISA检测肺组织花生四烯酸含量;支气管-肺泡灌洗液嗜中性粒细胞计数、肺组织髓过氧化物酶活性、肺干/湿重比值和肺组织学评分用于反映肺损伤的严重程度。结果单纯给予溶剂未对实验动物造成明显副作用。给予AACOCF3或PDTC,但未行单肺通气的实验动物除C-PLA2或NF-κB明显下调外(P<0.05),其余指标无显著变化。单肺通气实验动物肺组织C-PLA2和NF-κB表达水平均显著上调(P<0.05),出现明显的肺损伤(P<0.05);AACOCF3或PDTC预处理均可显著降低单肺通气实验动物肺组织C-PLA2和NF-κB表达水平(P<0.05),同时肺损伤程度明显减轻(P<0.05)。结论 C-PLA2和NF-κB在单肺通气致肺损伤中均发挥重要作用,二者相互调控,相互影响。Objective To elucidate the mechanisms of up-regulated expression of cytoplasmic phospholipase A2(C-PLA2)induced by one-lung ventilation(OLV) by investigating the interactions between nuclear factor-kappa B(NF-κB) and C-PLA2.Methods Forty-eight healthy Japanese white rabbits were randomized into control group,solvent treatment group(group S),NF-κB inhibitor(PDTC)/solvent treatment group(group PS),C-PLA2 inhibitor(AACOCF3)/solvent treatment group(group AS),OLV group(group O),solvent treatment plus OLV group(SO group),NF-κB inhibitor(PDTC)/solvent treatment plus OLV group(group PSO) and C-PLA2 inhibitor(AACOCF3)/solvent treatment plus OLV group(group ASO).ELISA was used to detect arachidonic acid(AA) content in the lung tissues,and NF-κB and C-PLA2 expressions were detected by Western blotting and quantitative PCR.Lung injuries were assessed based on the lung histological score,and the polymorphonuclear leukocyte count in the bronchial-alveolar lavage fluid,myeloperoxidase(MPO) content in the lung tissues,and lung wet/dry weight(W/D) raito were determined.Results Treatment of the rabbits with the solvent did not produce any adverse effects.OLV caused obvious lung injury in the rabbits and up-regulated the expressions of C-PLA2 and NF-κB in the lung tissues(P〈0.05).In rabbits without OLV,treatment with AACOCF3 or PDTC significantly down-regulated both C-PLA2 and NF-κB expressions without affecting the other parameters.In rabbits with OLV,treatment with AACOCF3 or PDTC obviously lowered C-PLA2 and NF-κB expressions and lessened the OLV-induced lung injuries.Conclusion Both C-PLA2 and NF-κB play important roles and show interactions in OLV-induced lung injury in rabbits.
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