Yamazaki Taisuke, Tukiyama Takashi, Tokiwa Takayoshi
Kohno Clinical Medicine Research Institute, 3-4-4, Kita-Shinagawa, Tokyo 140-0001, Japan.
In Vitro Cell Dev Biol Anim. 2005 Mar-Apr;41(3-4):80-2. doi: 10.1290/0502011.1.
Previously, we showed that dexamethasone (DEX) inhibited the expression of inflammatory cytokines, matrix metalloproteinase-1, and cyclooxygenase-2 messenger ribonucleic acid in SW982 cells. In this study, the effect of DEX on the transcription factors nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) was examined in SW982 cells by electrophoretic mobility shift assay (EMSA). Both NF-kappaB and AP-1 deoxyribonucleic acid binding activities were detectable in SW982 cells by EMSA, and they were induced by interleukin-1beta treatment. DEX inhibited NF-kappaB binding activity at 10 microM as well as at 100 microM, although the inhibition was only partial. However, DEX had little effect on AP-1 activity. These results suggest that DEX reduces the expression of inflammatory cytokines and other proteins in SW982 cells by inhibiting NF-kappaB.
此前,我们发现地塞米松(DEX)可抑制SW982细胞中炎性细胞因子、基质金属蛋白酶-1和环氧化酶-2信使核糖核酸的表达。在本研究中,通过电泳迁移率变动分析(EMSA)检测了DEX对SW982细胞中转录因子核因子-κB(NF-κB)和活化蛋白-1(AP-1)的影响。通过EMSA可在SW982细胞中检测到NF-κB和AP-1的脱氧核糖核酸结合活性,且它们可被白细胞介素-1β处理诱导。DEX在10微摩尔以及100微摩尔时均可抑制NF-κB结合活性,尽管这种抑制只是部分性的。然而,DEX对AP-1活性几乎没有影响。这些结果表明,DEX通过抑制NF-κB来降低SW982细胞中炎性细胞因子和其他蛋白质的表达。