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机构地区:[1]山西医科大学第一医院呼吸科,太原030001
出 处:《国际呼吸杂志》2010年第16期961-964,共4页International Journal of Respiration
基 金:山西省科技攻关资助项目(2007032016-1);太原市科技资助项目(0801041)
摘 要:目的 通过观察不同潮气量机械通气大鼠肺组织核因子κB(NF κB)p65蛋白和巨噬细胞炎症蛋白-1 α(MIP-1α)mRNA表达水平,探讨NF-κB活化对呼吸机致急性肺损伤大鼠肺组织MIP-1α表达的调控作用.方法 24只雄性健康Wistar大鼠随机分为对照组、小潮气量组和大潮气量组.分别采用原位杂交和免疫组织化学染色法检测各组大鼠肺组织MIP-1α mRNA及NF-κB p65蛋白的表达水平.结果 大潮气量组大鼠肺组织细支气管上皮NF-κB p65蛋白和MIP-1α mRNA阳性表达细胞百分比均明显高于小潮气量组和对照组(P值均〈0.01).对照组与小潮气量组比较差异无统计学意义.相关性分析结果表明,各组大鼠细支气管上皮NF-κB p65蛋白阳性表达细胞百分比与MIP-1α mRNA阳性表达细胞百分比之间呈正相关(r=0.482,P〈0.05).结论 大潮气量机械通气引发肺组织MIP-1α mRNA高表达在呼吸机所致肺损伤发生中具有一定作用,肺组织MIP 1α表达在一定程度上可能受NF-κB的调控.Objective To approach the regulating role of nuclear factor KB (NF-κB) in macrophage inflammatory protein-1α (MIP-1α) expression in lung of rats with ventilator induced acute lung injury by observing the expressions of NF-κB p65 protein and MIP-1α mRNA in lung of rats with different tidal volumes of ventilation. Methods Twenty-four health male Wistar rats were randomly divided into control group,low tidal volume group and high tidal volume group. The expressions of MIP-1α mRNA and NF-κB p65 protein in lung tissue of rats were detected with hybridization in situ and immunohistochemistry respectively. Results The positive percentages of expressions of NF-κB p65 protein and MIP-1α mRNA in bronchiole epithelial cells of rats in high tidal volume group were significantly higher than those in low tidal volume group and control group (all P 〈0. 01). There was no statistical significance between low tidal volume group and control group. Correlation analysis showed that the positive percentage of NF-κB p65 protein expression was positively correlated with that of MIP-1α mRNA expression in bronchiole epithelial cells of all groups ( r =0. 482, P 〈0. 05). Conclusions The high-expression of MIP-1α mRNA in lung tissue initiated by high tidal volume ventilation has certain effect on ventilator induced lung injury, and to some extent,the expression of MIP-1α in lung tissues may be regulated by NF-κB.
关 键 词:机械通气 急性肺损伤 核因子ΚB 巨噬细胞炎症蛋白-1Α
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