摘要
目的 :探讨一氧化氮 (NO)在内毒素刺激肺泡巨噬细胞 (PAM)对核因子κB(NFκB)活性的影响。方法 :用支气管肺泡灌洗法收集 PAM进行培养 ,分正常对照组、脂多糖 (L PS)组和 NO+L PS组。用凝胶电泳迁移率改变分析 (EMSA)法和酶联免疫吸附 (EL ISA)法分别检测核提取物中 NFκB活性和细胞培养上清中肿瘤坏死因子 α(TNFα)含量。结果 :L PS组 NFκB活性和 TNFα含量在刺激后 1小时明显高于正常对照组 ;NO+L PS组 NFκB活性和 TNFα含量在刺激后 1小时均显著低于 L PS组。结论 :L PS诱导 PAM的NFκB活化 ,导致 TNFα大量释放 ;NO可抑制 NFκB活化而减少
Objective:To investigate activation of nuclear factorκB(NFκB) in pulmonary alveolar macrophages(PAM) by nitric oxide(NO) in lipopolysaccharide induced acute lung injury.Methods:PAM collected from bronchoalveolar lavage fluid(BALF) were cultured and divided into 3 groups:control group,lipopolysaccharide(LPS) stimulated group,NO+LPS group.The NFκB activity of nuclear protein extract from the PAM and the concentration of tumor necrosis factorα(TNFα) in the supernatant were measured by electrophoretic mobility shift assay(ESMA) and enzymelinked immunosorbent assay(ELISA).Results:The activity of NFκB and the level of TNFα significantly increased after 1 hour by LPS stimulation. Compared with LPS stimulated group,both NFκB activity and concentration of TNFα were significantly lowered in NO+LPS group after 1 hour.Conclusions:LPS might activate NFκB in the PAMs and induce the increase of transcription and expression of TNFα gene.NO could inhibit the activation of NFκB and reduce the release of TNFα.
出处
《中国危重病急救医学》
CAS
CSCD
2002年第9期537-539,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目 (No.3 0 0 0 0 165 )
