国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2010年
16期
961-964
,共4页
机械通气%急性肺损伤%核因子κB%巨噬细胞炎症蛋白-1α
機械通氣%急性肺損傷%覈因子κB%巨噬細胞炎癥蛋白-1α
궤계통기%급성폐손상%핵인자κB%거서세포염증단백-1α
Mechanical ventilation%Acute lung injury%Nuclear factor-κB%Macrophage inflammatory protein-1α
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.
目的 通過觀察不同潮氣量機械通氣大鼠肺組織覈因子κB(NF κB)p65蛋白和巨噬細胞炎癥蛋白-1 α(MIP-1α)mRNA錶達水平,探討NF-κB活化對呼吸機緻急性肺損傷大鼠肺組織MIP-1α錶達的調控作用.方法 24隻雄性健康Wistar大鼠隨機分為對照組、小潮氣量組和大潮氣量組.分彆採用原位雜交和免疫組織化學染色法檢測各組大鼠肺組織MIP-1α mRNA及NF-κB p65蛋白的錶達水平.結果 大潮氣量組大鼠肺組織細支氣管上皮NF-κB p65蛋白和MIP-1α mRNA暘性錶達細胞百分比均明顯高于小潮氣量組和對照組(P值均<0.01).對照組與小潮氣量組比較差異無統計學意義.相關性分析結果錶明,各組大鼠細支氣管上皮NF-κB p65蛋白暘性錶達細胞百分比與MIP-1α mRNA暘性錶達細胞百分比之間呈正相關(r=0.482,P<0.05).結論 大潮氣量機械通氣引髮肺組織MIP-1α mRNA高錶達在呼吸機所緻肺損傷髮生中具有一定作用,肺組織MIP 1α錶達在一定程度上可能受NF-κB的調控.
목적 통과관찰불동조기량궤계통기대서폐조직핵인자κB(NF κB)p65단백화거서세포염증단백-1 α(MIP-1α)mRNA표체수평,탐토NF-κB활화대호흡궤치급성폐손상대서폐조직MIP-1α표체적조공작용.방법 24지웅성건강Wistar대서수궤분위대조조、소조기량조화대조기량조.분별채용원위잡교화면역조직화학염색법검측각조대서폐조직MIP-1α mRNA급NF-κB p65단백적표체수평.결과 대조기량조대서폐조직세지기관상피NF-κB p65단백화MIP-1α mRNA양성표체세포백분비균명현고우소조기량조화대조조(P치균<0.01).대조조여소조기량조비교차이무통계학의의.상관성분석결과표명,각조대서세지기관상피NF-κB p65단백양성표체세포백분비여MIP-1α mRNA양성표체세포백분비지간정정상관(r=0.482,P<0.05).결론 대조기량궤계통기인발폐조직MIP-1α mRNA고표체재호흡궤소치폐손상발생중구유일정작용,폐조직MIP 1α표체재일정정도상가능수NF-κB적조공.
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.
