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Anti-inflammatory effect of Apo-9 '-fucoxanthinone via inhibition of MAPKs and NF-kB signaling pathway in LPS-stimulated RAW 264.7 macrophages and zebrafish model

机译:通过抑制MAPK和NF-KB信号通路的抗炎作用,LPS刺激的原料264.7巨噬细胞和斑马鱼模型

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摘要

In this study, we confirmed the anti-inflammatory effect of Apo-9-fucoxanthinone (AF) in in vitro RAW 264.7 cells and in vivo zebrafish model. In lipopolysaccharide (LPS)-stimulated zebrafish, AF significantly decreased the production of reactive oxygen species (ROS), nitric oxide (NO) and cell death. In addition, the mRNA expression of inducible nitric oxide synthase (iNOS), suppressed cyclooxygenase-2 (COX-2) and an inflammatory cytokines; IL-1 beta, TNF-alpha were shown reduction. And AF significantly inhibited NO production and expression of iNOS in LPS-stimulated RAW 264.7 cells. Further, AF suppressed COX-2, prostaglandin E2 (PGE2), and pro-inflammatory cytokines such as interleukin-6 (IL-6), IL-1 beta and tumor necrosis factor-alpha (TNF-alpha) at 25, 50 and 100 mu g/mL, respectively. Further mechanistic studies showed that AF suppressed the nuclear factor-kB (NF-kB) pathway and phosphorylation of mitogen-activated protein kinase (MAPK) pathway molecules such as extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). According to the results, AF can be used and applied as a useful anti-inflammatory agent of nutraceutical or pharmaceutical.
机译:在这项研究中,我们证实了APO-9-豆豆酮(AF)在体外原始264.7细胞和体内斑马鱼模型中的抗炎作用。在脂多糖(LPS)刺激的斑马鱼中,AF显着降低了活性氧(ROS),一氧化氮(NO)和细胞死亡的产生。另外,诱导型一氧化氮合酶(InOS)的mRNA表达,抑制环加氧基酶-2(COX-2)和炎性细胞因子;显示IL-1β,TNF-α显示减少。和AF显着抑制LPS刺激的原料264.7细胞中InOS的生产和表达。此外,AF抑制的COX-2,前列腺素E2(PGE2)和促炎细胞因子,如白细胞介素-6(IL-6),IL-1β和肿瘤坏死因子-α(TNF-α),50和50分别为100μg/ ml。进一步的机械研究表明,AF抑制了核因子-KB(NF-KB)途径和丝裂解蛋白激酶(MAPK)途径分子的磷酸化,例如细胞外信号调节激酶(ERK)和C-JUM N-末端激酶( JNK)。根据结果​​,可以使用AF作为营养保健品或药物的有用抗炎剂。

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