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核因子-κB(NF-κB)和活化蛋白-1(AP-1)在姜黄素和吡咯烷二硫代氨基甲酸盐对紫外线B(UVB)诱导的角质形成细胞细胞因子表达的调节中的相对作用。

Relative contribution of NF-kappaB and AP-1 in the modulation by curcumin and pyrrolidine dithiocarbamate of the UVB-induced cytokine expression by keratinocytes.

作者信息

Grandjean-Laquerriere Alexia, Gangloff Sophie C, Le Naour Richard, Trentesaux Chantal, Hornebeck William, Guenounou Moncef

机构信息

Laboratoire d'Immunologie (EA2070), IFR 53 Biomolécules, INSERM, CNRS, 1 avenue du Maréchal Juin, 51100, Reims, France.

出版信息

Cytokine. 2002 May 7;18(3):168-77. doi: 10.1006/cyto.2002.0888.

Abstract

Following ultraviolet B treatment, expression of tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 by NCTC 2544 keratinocyte cell line was significantly enhanced both at the mRNA and protein level. The UVB also increased the IL-10 steady-state mRNAs level. Radiation-induced cytokine overexpression was accompanied by NF-kappaB and AP-1 transcription factors activation as assessed by electrophoretic mobility shift assays. To investigate in keratinocytes the relative contributions of those transcription factors on UVB-mediated cytokine induction, cell cultures were supplemented with curcumin and pyrrolidine dithiocarbamate (PDTC), agents known to modulate NF-kappaB and AP-1 activation. Both compounds significantly inhibited NF-kappaB activation by UVB, but AP-1 activation was unaffected by curcumin while PDTC further stimulated its activation. In parallel, curcumin decreased, in a dose-dependent manner, the UVB-mediated overexpression of all three pro-inflammatory cytokines and only exhibited a moderate enhancing influence on IL-10 expression. In turn, the inhibitory influence of PDTC on radiation-induced TNF-alpha and IL-6 expression is much lower and in contrast to curcumin, it stimulated IL-8. Taken together, our data indicated that control of proinflammatory cytokine expression induced by UVB in keratinocytes required the selective inhibition of NF-kappaB activation. Simultaneous AP-1 activation by agents like PDTC might, partially or totally, depending on cytokine-type, counterbalanced the inhibitory effect exerted on UVB-induced NF-kappaB activation in keratinocytes.

摘要

在紫外线B(UVB)处理后,NCTC 2544角质形成细胞系中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和IL-8在mRNA和蛋白质水平上的表达均显著增强。UVB还增加了IL-10的稳态mRNA水平。通过电泳迁移率变动分析评估,辐射诱导的细胞因子过表达伴随着核因子κB(NF-κB)和活化蛋白-1(AP-1)转录因子的激活。为了研究在角质形成细胞中这些转录因子对UVB介导的细胞因子诱导的相对贡献,细胞培养物中添加了姜黄素和吡咯烷二硫代氨基甲酸盐(PDTC),这两种物质已知可调节NF-κB和AP-1的激活。两种化合物均显著抑制UVB诱导的NF-κB激活,但姜黄素对AP-1激活无影响,而PDTC进一步刺激其激活。同时,姜黄素以剂量依赖的方式降低了UVB介导的所有三种促炎细胞因子的过表达,并且仅对IL-10表达表现出适度的增强作用。相反,PDTC对辐射诱导的TNF-α和IL-6表达的抑制作用要低得多,并且与姜黄素不同,它刺激了IL-8。综上所述,我们的数据表明,控制角质形成细胞中UVB诱导的促炎细胞因子表达需要选择性抑制NF-κB激活。像PDTC这样的物质同时激活AP-1可能会部分或完全(取决于细胞因子类型)抵消对角质形成细胞中UVB诱导的NF-κB激活所施加的抑制作用。

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