Guo G, Wang H
Department of Nephrology, First Hospital, Beijing Medical University.
Zhonghua Yi Xue Za Zhi. 1998 Apr;78(4):290-2.
To study the regulative effect of nuclear factor kappa B (NF-kappa B) on the expression of intercellular adhesion molecular-1(ICAM-1) in human mesangial cells (HMC) by interleukin I-1 beta (IL-1 beta).
Activation of NF-kappa B was measured by electrophoresis mobility shift assay (EMSA). ICAM-1 expression was detected by Northern Blot and Cell ELISA.
rhIL-1 beta (10 ng/ml) could rapidly stimulate activation and translocation of NF-kappa B, and also could enhance the expression of ICAM-1 in mRNA (0.14 vs 0.35) and protein (0.92 +/- 0.10 vs 1.35 +/- 0.11, P < 0.01) level. After pretreatment with 100 mumol/L L-1-chlor-3-(4-tosylamido)-4-phenyl-2 butanon (TPCK), an inhibitor of NF-kappa B, both ICAM-1 levels of mRNA and protein stimulated by rhIL-1 beta were blocked by about 50% in these cells (0.46 +/- 0.05 vs 1.29 +/- 0.12, P < 0.01) compared with the rhIL-1 beta-stimulated group.
These results suggest that NF-kappa B 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.
研究核因子κB（NF-κB）对白细胞介素I-1β（IL-1β）刺激下人系膜细胞（HMC）细胞间黏附分子-1（ICAM-1）表达的调节作用。
采用电泳迁移率变动分析（EMSA）检测NF-κB的激活情况。通过Northern印迹和细胞酶联免疫吸附测定法检测ICAM-1的表达。
重组人白细胞介素-1β（rhIL-1β，10 ng/ml）能迅速刺激NF-κB的激活和转位，同时还能增强ICAM-1在mRNA（0.14对0.35）和蛋白（0.92±0.10对1.35±0.11，P<0.01）水平的表达。用100 μmol/L的NF-κB抑制剂L-1-氯-3-（4-甲苯磺酰胺基）-4-苯基-2-丁酮（TPCK）预处理后，与rhIL-1β刺激组相比，rhIL-1β刺激的这些细胞中ICAM-1的mRNA和蛋白水平均被阻断约50%（0.46±0.05对1.29±0.12，P<0.01）。
这些结果表明，NF-κB是IL-1刺激HMC中ICAM-1表达的信号因子之一。它可能参与调节肾小球疾病中的免疫炎症过程。
