首页> 美国卫生研究院文献>Mediators of Inflammation >Davallia mariesii Moore Improves FcεRI-Mediated Allergic Responses in the Rat Basophilic Leukemia Mast Cell Line RBL-2H3 and Passive Cutaneous Anaphylaxis in Mice
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Davallia mariesii Moore Improves FcεRI-Mediated Allergic Responses in the Rat Basophilic Leukemia Mast Cell Line RBL-2H3 and Passive Cutaneous Anaphylaxis in Mice

机译:滨海黄val改善大鼠嗜碱性粒细胞肥大细胞系RBL-2H3和小鼠被动皮肤过敏反应中FcεRI介导的过敏反应。

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摘要

Davallia mariesii Moore (Drynaria rhizome extract (DRE)) is widely known for its efficacy in treating inflammation, arteriosclerosis, and bone injuries. This study evaluated whether treatment with DRE inhibited FcɛRI-mediated allergic responses in the RBL-2H3 mast cells and investigated the early- and late-phase mechanisms by which DRE exerts its antiallergic effects. IgE anti-DNP/DNP-HSA-sensitized RBL-2H3 mast cells were tested for cytotoxicity to DRE, followed by the assessment of β-hexosaminidase release. We measured the amounts of inflammatory mediators (e.g., histamine, PGD2, TNF-α, IL-4, and IL-6) and examined the expression of genes involved in arachidonate and FcεRI signaling pathways. In addition, we confirmed the antiallergic effects of DRE on passive cutaneous anaphylaxis (PCA) in mice. DRE inhibited RBL-2H3 mast cell degranulation and production of allergic mediators in them. In early allergic responses, DRE reduced expression of FcεRI signaling-related genes (e.g., Syk, Lyn, and Fyn) and extracellular signal-regulated kinase phosphorylation in mast cells. In late allergic responses, DRE reduced PGD2 release and COX-2 expression and cPLA2 phosphorylation in FcɛRI-mediated mast cells. Lastly, 250–500 mg/kg DRE significantly attenuated the IgE-induced PCA reaction in mice. These findings provide novel information on the molecular mechanisms underlying the antiallergic effects of DRE in FcɛRI-mediated allergic responses.
机译:沿海大黄藻(Davallia mariesii Moore)(Drynaria根茎提取物(DRE))以治疗炎症,动脉硬化和骨骼损伤的功效而广为人知。这项研究评估了DRE处理是否能抑制RBL-2H3肥大细胞中FcɛRI介导的过敏反应,并研究了DRE发挥其抗过敏作用的早期和晚期机制。测试了IgE抗DNP / DNP-HSA致敏的RBL-2H3肥大细胞对DRE的细胞毒性,然后评估了β-己糖胺酶的释放。我们测量了炎性介质(例如组胺,PGD2,TNF-α,IL-4和IL-6)的数量,并检查了涉及花生四烯酸和FcεRI信号通路的基因的表达。此外,我们证实了DRE对小鼠被动皮肤过敏反应(PCA)的抗过敏作用。 DRE抑制RBL-2H3肥大细胞脱粒和其中的过敏介质的产生。在早期的过敏反应中,DRE减少了肥大细胞中FcεRI信号相关基因(例如Syk,Lyn和Fyn)的表达以及细胞外信号调节的激酶磷酸化。在晚期过敏反应中,DRE降低了FcɛRI介导的肥大细胞中PGD2的释放和COX-2的表达以及cPLA2的磷酸化。最后,250-500 mg / kg DRE显着减弱了小鼠IgE诱导的PCA反应。这些发现提供了有关DRE在FcmediatedRI介导的过敏反应中抗过敏作用的分子机制的新信息。

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