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首页> 外文期刊>Archives of pharmacal research >Atractylodes japonica Koidzumi inhibits the production of proinflammatory cytokines through inhibition of the NF-kappaB/IkappaB signal pathway in HMC-1 human mast cells.
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Atractylodes japonica Koidzumi inhibits the production of proinflammatory cytokines through inhibition of the NF-kappaB/IkappaB signal pathway in HMC-1 human mast cells.

机译:苍术通过抑制HMC-1人肥大细胞中的NF-κB/ IkappaB信号通路来抑制促炎细胞因子的产生。

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摘要

The rhizome of Atractylodes japonica Koidzumi (AJK) has been used in traditional medicine for treatment of arthritis, bronchitis and respiratory infectious disease, whereas its effects on inflammatory reactions have not been unknown recently. In this study, the effects of AJK on allergic inflammation and its signaling were investigated in the induced human mast cells and animal model. This study showed that ethanol extract of AJK interestingly suppressed the production and mRNA expression of TNF-alpha, IL-6 and IL-8, as important inflammatory cytokines. Furthermore, AJK inhibited the nuclear translocation of nuclear factor (NF)-kappaB through inhibition of the phosphorylation of IB-kappa, which was additionally elucidated by NF-kappaB promoter-mediated luciferase activity. In addition, the phosphorylation of ERK was increased in pretreatment with AJK, whereas there was no change in JNK and p38 MAPK. However, AJK showed no effects on anti-DNP IgE-mediated in vivo PCA reaction and histamine release, as key events of mast cell-mediated immediate allergic reactions. These results suggest that AJK might be involved in not early-phase but transition to late-phase reactions of allergic inflammation and could modulate through other signal pathways. Taken together, AJK could be used as a treatment for mast cell mediated late-phase/chronic allergic inflammatory reactions.
机译:日本白术的根茎(AJK)已被用于治疗关节炎,支气管炎和呼吸道感染性疾病的传统医学中,但其对炎症反应的影响最近尚不明确。在这项研究中,在诱导的人肥大细胞和动物模型中研究了AJK对过敏性炎症及其信号传导的影响。这项研究表明,AJK的乙醇提取物有趣地抑制了TNF-α,IL-6和IL-8的产生和mRNA表达,这是重要的炎症细胞因子。此外,AJK通过抑制IB-kappa的磷酸化而抑制了核因子(NF)-kappaB的核易位,而NF-kappaB启动子介导的萤光素酶活性进一步阐明了该磷酸化。此外,在用AJK预处理后,ERK的磷酸化增加,而JNK和p38 MAPK没有变化。然而,作为肥大细胞介导的立即变态反应的关键事件,AJK对抗DNP IgE介导的体内PCA反应和组胺释放没有影响。这些结果表明,AJK可能不参与过敏性炎症的早期反应,而是过渡到晚期反应,并可能通过其他信号途径进行调节。两者合计,AJK可用作肥大细胞介导的晚期/慢性过敏性炎症反应的治疗方法。

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