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[艾拉莫德对脂多糖刺激的大鼠肺泡巨噬细胞系中肿瘤坏死因子α产生及核因子κB活性的抑制作用]

[Inhibitory effect of iguratimod on TNFalpha production and NF-kappaB activity in LPS-stimulated rat alveolar macrophage cell line].

作者信息

Jiang Ye, Lü Wei, Yu Shu-Qin, Yao Lin, Xu Guang-Lin, Zhang Xi-Ran

机构信息

Center for New Drug Research and Development, Jiangsu Key Laboratory for Molecular Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210097, China.

出版信息

Yao Xue Xue Bao. 2006 May;41(5):401-5.

Abstract

AIM

To investigate the effect of iguratimod (T-614), a non-steroidal anti-inflammatory drug, on TNFalpha mRNA expression and TNFalpha production, and on the activity of nuclear factor-kappaB (NF-kappaB) 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 micromol x L(-1)), then were stimulated with LPS. The production of TNFalpha in the supernatant of NR8383 was assayed by enzyme-linked immunosorbent assay (ELISA). The TNFalpha mRNA level was determined by a semi-quantitative PCR assay. Assessment of the NF-kappaB DNA binding activity was performed by an ELISA kit.

RESULTS

T-614 inhibited LPS-stimulated mRNA expression and production of TNFalpha in a concentration-dependent manner, as well as the activity of NF-kappaB. The IC50 value of effect of T-614 on TNFalpha level was 26.2 micromol x L(-1).

CONCLUSION

The inhibitory effect of T-614 on the production of TNFalpha in LPS-stimulated NR8383 cells may be mediated by suppression of NF-kappaB activity.

摘要

目的

研究非甾体抗炎药艾拉莫德(T-614)对脂多糖(LPS)激活的大鼠肺泡巨噬细胞系(NR8383)中肿瘤坏死因子α(TNFα)mRNA表达、TNFα产生以及核因子κB(NF-κB)活性的影响。

方法

NR8383细胞先用T-614(13.4、26.7、53.4 μmol·L⁻¹)预处理,然后用LPS刺激。采用酶联免疫吸附测定(ELISA)法检测NR8383细胞上清液中TNFα的产生。通过半定量聚合酶链反应(PCR)测定法确定TNFα mRNA水平。使用ELISA试剂盒评估NF-κB DNA结合活性。

结果

T-614以浓度依赖性方式抑制LPS刺激的TNFα mRNA表达和产生,以及NF-κB的活性。T-614对TNFα水平影响的半数抑制浓度(IC50)值为26.2 μmol·L⁻¹。

结论

T-614对LPS刺激的NR8383细胞中TNFα产生的抑制作用可能是通过抑制NF-κB活性介导的。

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