目的：探讨NF-κB信号途径在新生鼠败血症中的作用,为临床寻求以NF-κB为靶点的治疗手段提供实验依据。方法：应用10 d新生大鼠制备金黄色葡萄球菌败血症模型。采用电泳迁移率改变分析(EMSA)方法检测败血症新生鼠肺脏NF-κB的表达情况和应用吡咯-硫氨基甲酸酯(PDTC)后肺脏NF-κB活性变化情况。结果：金黄色葡萄球菌败血症新生鼠的肺脏NF-κB活性于注菌后1 h开始增强,3 h达高峰。PDTC对肺脏NF-κB活化有抑制作用,且剂量越大,抑制作用越强。结论：新生鼠金黄色葡萄球菌败血症时肺脏NF-κB有明显激活,且存在一高峰期。抗氧化剂PUTC能对金黄色葡萄球菌败血症新生鼠肺脏NF-κB活化有所抑制,且存在量-效依赖关系。

OBJECTIVE: To study the role of NF-κB signal pathway in neonatal rats with sepsis so as to provide the experimental base for corresponding clinical treatment of sepsis, in which NF-icB is taken as the target. METHODS: The sepsis model was established by injecting staphylococcus aureus subcutaneously in 10-day-old newborn rats. The activity of NF-icB in the lungs of newborn rats with staphylococcus aureus sepsis was detected by the electrophoretic mobility shift assay (EMSA) and the effect of anti-oxidant pyrrolidine dithiocarbamate (PDTC) on it was studied. RESULTS: In newborn rats with staphylococcus aureus sepsis, the activity of lung NF-κB was enhanced at the 1st h and reached a peak at the 3rd h after injection of staphylococcus aureus. PDTC had an inhibitive effect on the activity of lung NF-κB. The larger the dosage, the more intensified the inhibitive effect. CONCLUSIONS: In newborn rats with staphylococcus aureus sepsis, the NF-κB of lungs is activated, and the activation of NF-κB has a peak. The anti-oxidant PDTC can inhibit lung NF-κB activity in a dose-effect way in newborn rats with staphylococcus aureus sepsis.