摘要
目的 :探讨白介素 10和外源性一氧化氮 (NO)对内毒素 (L PS)诱导肺泡巨噬细胞 (PAM)核因子 κB(NFκB)活化及肿瘤坏死因子 α(TNFα)基因表达的调节 ,为临床运用提供理论依据。方法 :用支气管肺泡灌洗法收集 PAM进行培养 ,分为正常对照组、L PS组、IL 10 +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TNFα含量。结果 :L PS组 NFκB活性和 TNFα含量在刺激后 3小时显著高于正常对照组 ;IL 10 +L PS组和 NO+L PS组 NFκB活性和 TNFα含量均显著低于 L PS组。结论 :L PS诱导 PAM的 NFκB活化 ,导致 TNFα基因表达增强 ;白介素 10和外源性 NO可抑制 NFκB活化而减少
Objective:To evaluate the effects of interleukin10(IL10) and nitric oxide(NO) on the activation of nuclear factorκB(NFκB) and the expression of tumor necrosis factorα(TNFα) in pulmonary alveolar macrophages(PAM) induced by lipopolysaccharide.Methods:PAM collected by bronchusassociated lymphoid tissue(BALT) were cultured and divided into 4 groups:control group;lipopolysaccharide(LPS)stimulated group;IL10+LPS group and NO+LPS group.The NFκB activity of nuclear protein extract from the PAM and the concentration of TNFα in the supernatant were measured with electrophoretic mobility shift assay (EMSA) and enzyme linked immunoadsorbent assay(ELISA),respectively.Results:The activity of NFκB and the level of TNFα significantly increased at 3 hour after LPS stimulation;compared with LPS stimulated group,both NFκB activity and concentration of TNFα were significantly lowered in IL10+LPS group and NO+LPS group.Conclusions:LPS might activity NFκB in the PAM and induce an increase in transcription and expression of TNFα gene.IL10 and 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
2001年第5期284-286,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目! (No.3 9770 73 6)
