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首页> 外文期刊>Inflammation >Norisoboldine Inhibits the Production of Pro-inflammatory Cytokines in Lipopolysaccharide-Stimulated RAW 264.7 Cells by Down-Regulating the Activation of MAPKs but Not NF-κB
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Norisoboldine Inhibits the Production of Pro-inflammatory Cytokines in Lipopolysaccharide-Stimulated RAW 264.7 Cells by Down-Regulating the Activation of MAPKs but Not NF-κB

机译：Norisoboldine通过下调MAPK而不是NF-κB的激活抑制脂多糖刺激的RAW 264.7细胞中促炎性细胞因子的产生

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Norisoboldine is the main isoquinoline alkaloid occurring in Radix Linderae, the dry roots of Lindera aggregata (Lauraceae family). It has been previously implicated to be able to ameliorate the synovial inflammation and abnormal immune conditions in collagen-induced arthritis of mice. To get insight to the potential anti-inflammatory mechanisms of this alkaloid compound, the present study was undertaken to explore the effects of norisoboldine on the production of pro-inflammatory cytokines from macrophages stimulated by lipopolysaccharide. In vitro, norisoboldine substantially reduced the production of nitric oxide (NO), tumor necrosis factor (TNF)-α as well as interleukin (IL)-1β from RAW264.7 macrophage cells in a concentration-dependent manner, whereas it only slightly reduced the production of interleukin-6 (IL-6) at both protein and transcription levels. Of note, the preventive effects of norisoboldine on the release of pro-inflammatory cytokines were correlated with the inhibitory action on the phosphorylations of mitogen-activated protein (MAP) kinases including p38, extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK), but not on the activation and translocation of nuclear factor-κB (NF-κB). It can be therefore concluded that norisoboldine inhibits the macrophage activation and the resultant production of pro-inflammatory cytokines via down-regulating the activation of MAPKs signaling pathways rather than NF-κB.
机译：Norisoboldine是林丹的主要异喹啉生物碱，林丹是灵芝（Lauraceae家族）的干燥根。先前已暗示其能够改善胶原蛋白诱发的小鼠的滑膜炎症和异常的免疫状况。为了深入了解这种生物碱化合物的潜在抗炎机制，进行了本研究以探讨去甲胆碱对脂多糖刺激的巨噬细胞产生促炎细胞因子的影响。在体外，去甲肾上腺素以浓度依赖的方式显着降低了RAW264.7巨噬细胞中一氧化氮（NO），肿瘤坏死因子（TNF）-α和白介素（IL）-1β的产生，但仅略有减少在蛋白质和转录水平上都产生白介素6（IL-6）。值得注意的是，去甲胆碱对促炎性细胞因子释放的预防作用与对促分裂原激活蛋白（MAP）激酶（包括p38，细胞外信号调节激酶（ERK）和c-jun NH）磷酸化的抑制作用相关。 2 -末端激酶（JNK），但不影响核因子-κB（NF-κB）的活化和转运。因此可以得出结论，去甲山ob碱通过下调MAPKs信号通路而不是NF-κB的活化来抑制巨噬细胞的活化和促炎性细胞因子的产生。

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