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核因子-κB调控白细胞介素1β刺激人肾小球系膜细胞表达细胞间粘附分子 被引量:21

Regulative effect of nuclear factor κB on the expression of intercellular adhesion molecular 1 in human mesangial cells
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摘要 目的研究核因子κB(NFκB)对白细胞介素1β(IL1β)引起的体外培养的人肾小球系膜细胞表达细胞间粘附分子(ICAM1)的基因调控机理。方法采用凝胶迁移率法观测NFκB的活化,以Northern杂交方法检测细胞间粘附分子的基因表达,用细胞ELISA法检测ICAM1蛋白水平的表达。结果rhIL1β10ng/ml刺激肾小球系膜细胞1、2、4小时,均引起NFκB活化,且1小时为最强。4小时,ICAM1mRNA表达水平上调035(刺激前为014)。结论细胞因子IL1β刺激人肾小球系膜细胞表达细胞间粘附分子是通过NFκB调控,NFκB可能参与调节肾小球疾病的免疫炎症的过程。 Objective To study the regulative effect of nuclear factor κB (NF κB) on the expression of intercellular adhesion molecular 1(ICAM 1) in human mesangial cells (HMC) by interleukin Ⅰ 1β (IL 1β). Methods Activation of NF κB was measured by electrophoresis mobility shift assay (EMSA). ICAM 1 expression was detected by Northern Blot and Cell ELISA. Results rhIL 1β (10 ng/ml) could rapidly stimulate activation and translocation of NF κB, and also could enhance the expression of ICAM 1 in mRNA (0.14vs 0.35) and protein (0.92±0 10 vs 1.35±0.11, P <0.01) level. After pretreatment with 100 μmol/L L 1 chlor 3 (4 tosylamido) 4 phenyl 2 butanon (TPCK), an inhibitor of NF κB, both ICAM 1 levels of mRNA and protein stimulated by rhIL 1β were blocked by about 50% in these cells (0.46±0.05 vs 1.29±0.12, P <0.01) compared with the rhIL 1β stimulated group. Conclusion These results suggest that NF κB is one of the signaling factors for IL 1 stimulated ICAM 1 expression in HMC. It may modulate the immune inflammatory process in glomerular diseases.
出处 《中华医学杂志》 CAS CSCD 北大核心 1998年第4期290-292,共3页 National Medical Journal of China
基金 国家自然科学基金
关键词 白细胞介素1 核因子KB 细胞粘着分子 肾小球疾病 Interleukin 1 NF kappaB Cell adhesion molecules
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参考文献3

  • 1杨斌,中华医学杂志,1996年,76卷,416页
  • 2Ding G,Am J Physiol,1993年,264卷,577页
  • 3谌贻璞,北京医科大学学报,1989年,21卷,335页

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