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首页> 外文期刊>International immunopharmacology >Safflower polysaccharides activate the transcription factor NF-kappaB via Toll-like receptor 4 and induce cytokine production by macrophages.
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Safflower polysaccharides activate the transcription factor NF-kappaB via Toll-like receptor 4 and induce cytokine production by macrophages.

机译:红花多糖通过Toll样受体4激活转录因子NF-κB,并诱导巨噬细胞产生细胞因子。

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摘要

Two active polysaccharide fractions (SF1 and SF2) purified from dried safflower petals (Carthamus tinctorius L.) stimulated the synthesis of various cytokines by peritoneal macrophages. In a number of cell types, SF1 and SF2 induced a rapid degradation of IkappaB alpha essential for the activation of the transcription factor NF-kappaB. Toll-like receptor 4 (TLR4), but not TLR2, was expressed in all cell lines that responded to SF1 and SF2. Enforced expression of TLR4 and MD-2 rendered responsiveness to SF1 and SF2. Moreover, these safflower polysaccharides failed to induce the production of TNF-alpha and NO by peritoneal macrophages prepared from C3H/HeJ mice that have a point mutation in the Tlr4 gene. Thus, these observations clearly indicate that safflower polysaccharides activate the NF-kappaB signaling pathway via TLR4.
机译:从干燥的红花花瓣(Carthamus tinctorius L.)中纯化得到的两个活性多糖级分(SF1和SF2)刺激了腹膜巨噬细胞合成各种细胞因子。在许多细胞类型中,SF1和SF2诱导了IkappaB alpha的快速降解,这对于激活转录因子NF-kappaB是必不可少的。 Toll样受体4(TLR4),但不是TLR2,在对SF1和SF2有反应的所有细胞系中表达。 TLR4和MD-2的强制表达使人对SF1和SF2有反应。而且,这些红花多糖不能诱导由在Tlr4基因中具有点突变的C3H / HeJ小鼠制备的腹膜巨噬细胞产生TNF-α和NO。因此,这些观察清楚地表明红花多糖通过TLR4激活NF-κB信号传导途径。

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