摘要
目的研究非甾体抗炎药艾拉莫德(T-614)对脂多糖(LPS)刺激的大鼠肺泡巨噬细胞系(NR8383)前炎症反应因子TNFα基因表达、蛋白合成的影响及其对核因子κB(NF-κB)的作用。方法体外培养NR8383经T-614(13.4,26.7及53.4μmol.L-1)处理,LPS刺激后应用酶联免疫吸附法(ELISA)检测细胞上清液中TNFα的水平,半定量逆转录聚合酶链式反应(RT-PCR)检测TNFαmRNA水平,ELISA法检测NF-κB的活性。结果T-614对LPS诱导的NR8383细胞TNFαmRNA水平和蛋白水平的上调有显著抑制作用,对NF-κB的转录活性也有抑制作用。结论T-614可能通过抑制LPS诱导的NR8383的NF-κB活性而降低TNFα的产生。
Aim To investigate the effect of iguratimod （T-614）, a non-steroidal anti-inflammatory drug, on TNFα mRNA expression and TNFα production, and on the activity of nuclear factor-κB （NF-κB） in the rat alveolar macrophage cell line （NR8383） activated by LPS. Methods NR8383 cells were pretreated with T-614 （13.4, 26.7, 53.4 μmol·L^-1）, then were stimulated with LPS. The production of TNFα in the supernatant of NR8383 was assayed by enzyme-linked immunosorbent assay （ELISA）. The TNFα mRNA level was determined by a semi-quantitative PCR assay. Assessment of the NF-κB DNA binding activity was performed by an ELISA kit. Results T-614 inhibited LPS-stimulated mRNA expression and production of TNFα in a concentration-dependent manner, as well as the activity of NF-κB. The IC50 value of effect of T-614 on TNFα level was 26.2 μmol·L^-1. Conclusion The inhibitory effect of T-614 on the production of TNFα in LPS-stimulated NR8383 cells may be mediated by suppression of NF-κB activity.
出处
《药学学报》
CAS
CSCD
北大核心
2006年第5期401-405,共5页
Acta Pharmaceutica Sinica
