摘要
目的 :探讨 IκB激酶 (IKK)在创伤性急性肺损伤 (AL I)病理变化中可能的作用机制。方法 :复制创伤性 AL I家兔模型 ,用原位杂交方法结合原位定量分析检测肺组织中 IKKβ的 m RNA表达 ,用凝胶电泳迁移率改变分析法 (EMSA)和酶联免疫吸附 (EL ISA)法分别检测肺泡巨噬细胞 (PAM)中核因子 κB(NFκB)的活性和 PAM培养上清液中 TNF a、IL 6的含量。结果 :创伤性 AL I家兔组肺组织中 IKKβ的 m RNA表达 (0 .10 6 3± 0 .0 2 18)以及 PAM中 NFκB活性 (2 987.85± 16 3.85 )和上清液中 TNF a、IL 6的含量〔分别为 (2 35 .6± 30 .8) ng/ L和 (398.8± 2 4 3.6 ) ng/ L〕均较正常对照组〔分别为 0 .0 4 2 7± 0 .0 2 4 1、92 2 .0 2± 2 8.36、(36 .4± 8.0 ) ng/ L和 (78.6± 39.4 ) ng/ L〕显著增高 (P均 <0 .0 1)。结论 :蛋白激酶 IKK的激活介导 NFκB活化和分泌高水平细胞因子在创伤性 AL I的炎症反应中发挥重要作用。
Objective:To investigate the possible mechanism of IκB kinase(IKK) in the pathogenesis of traumatic acute lung injury(ALI).Methods:Rabbit model of traumatic ALI was used in this study.In situ hybridization combined with in situ quantitative analysis was used to detect the IKKβ mRNA expression of lung tissue.The nuclear factorkappa B(NFκB) activity of nuclear protein extract from the pulmonary alveolar macrophage(PAM) and the concentration of tumor necrosis factorα(TNFα),interleukin6 ( IL6 ) in the supernatant were measured by electrophoretic mobility shift assay(EMSA) and enzyme linked immuno adsorbent assay(ELISA) respectively.Results:In traumatic ALI group,the expression of IKKβ mRNA was 0 106 3±0 021 8,the activity of NFκB was 2 987 85±163 85,the levels of TNFα and IL6 were (235 6±30 8) ng/L and (398 8±243 6) ng/L, and they were significantly higher than those of normal group〔0 042 7±0 024 1,922 02±28 36,(36 4±8 0) ng/L and (78 6±39 4) ng/L respectively, P <0 05 or P <0 01〕.Conclusions:The IKKβ expression,NFκB activation and cytokine secretion may play an important role in inflammatory reaction of traumatic ALI.
出处
《中国危重病急救医学》
CAS
CSCD
2002年第12期716-718,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目 (No.30 0 0 0 1 65
39770 736)
