首页> 美国卫生研究院文献>International Journal of Molecular Sciences >δ-Tocotrienol Isolated from Rice Bran Exerts an Anti-Inflammatory Effect via MAPKs and PPARs Signaling Pathways in Lipopolysaccharide-Stimulated Macrophages
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δ-Tocotrienol Isolated from Rice Bran Exerts an Anti-Inflammatory Effect via MAPKs and PPARs Signaling Pathways in Lipopolysaccharide-Stimulated Macrophages

机译:从米糠中分离出的δ-生育三烯酚通过脂多糖刺激的巨噬细胞中的MAPKs和PPARs信号传导途径发挥抗炎作用

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摘要

δ-Tocotrienol, an important component of vitamin E, has been reported to possess some physiological functions, such as anticancer and anti-inflammation, however their molecular mechanisms are not clear. In this study, δ-tocotrienol was isolated and purified from rice bran. The anti-inflammatory effect and mechanism of δ-tocotrienol against lipopolysaccharides (LPS) activated pro-inflammatory mediator expressions in RAW264.7 cells were investigated. Results showed that δ-tocotrienol significantly inhibited LPS-stimulated nitric oxide (NO) and proinflammatory cytokine (TNF-α, IFN-γ, IL-1β and IL-6) production and blocked the phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinases 1/2 (ERK1/2). δ-Tocotrienol repressed the transcriptional activations and translocations of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1), which were closely related with downregulated cytokine expressions. Meanwhile, δ-tocotrienol also affected the PPAR signal pathway and exerted an anti-inflammatory effect. Taken together, our data showed that δ-tocotrienol inhibited inflammation via mitogen-activated protein kinase (MAPK) and peroxisome proliferator-activated receptor (PPAR) signalings in LPS-stimulated macrophages.
机译:δ-生育三烯酚是维生素E的重要成分,据报道具有某些生理功能,例如抗癌和抗炎作用,但其分子机制尚不清楚。在这项研究中,从米糠中分离和纯化了δ-生育三烯酚。研究了δ-生育三烯酚对脂多糖(LPS)激活的RAW264.7细胞中促炎介质表达的抗炎作用和机制。结果显示δ-生育三烯酚显着抑制LPS刺激的一氧化氮(NO)和促炎细胞因子(TNF-α,IFN-γ,IL-1β和IL-6)的产生,并阻止c-Jun N端激酶( JNK)和细胞外调节蛋白激酶1/2(ERK1 / 2)。 δ-生育三烯酚抑制了核因子-κB(NF-κB)和激活蛋白-1(AP-1)的转录激活和易位,这与下调细胞因子的表达密切相关。同时,δ-生育三烯酚也影响PPAR信号通路并发挥抗炎作用。两者合计,我们的数据表明,δ-生育三烯酚通过LPS刺激的巨噬细胞中的促分裂原激活的蛋白激酶(MAPK)和过氧化物酶体增殖物激活的受体(PPAR)信号传导抑制炎症。

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