Yeyoung Kim, Soyoung Lee, Meiling Jin, Young-Ae Choi, Jin Kyeong Choi, Taeg Kyu Kwon, Dongwoo Khang, Sang-Hyun Kim
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Oral administration of ASP dose-dependently suppressed immunoglobulin (Ig)E-mediated PCA responses evidenced by Evans blue extravasation, ear thickening, and mast cell degranulation. ASP also significantly mitigated ovalbumin-induced ASA responses, including hypothermia, histamine secretion, and the production of IgE and interleukin-4. Notably, ASP was more effective in suppressing allergic inflammation than nothofagin, another prominent flavonoid known as an anti-allergic component of rooibos. The regulatory mechanism of mast cell activation by ASP was clarified using mast cell line and primary cultured mast cells (RBL-2H3 and mouse bone marrow-derived mast cells). ASP reduced IgE-stimulated mast cells degranulation and intracellular calcium influx by the inhibition of FcεRI signaling pathway (Lyn, Fyn, and Syk). Moreover, ASP reduced pro-inflammatory cytokine expressions by inhibiting two major transcription factors, nuclear factor of activated T cells and nuclear factor-κB. 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引用次数: 0
摘要
肥大细胞是通过释放组胺和促炎细胞因子等各种过敏介质引发过敏性炎症的初级细胞。阿斯巴拉汀(ASP)是路依布斯中独有的主要类黄酮,路依布斯是一种传统用于缓解过敏治疗的草药。在本研究中,我们探讨了 ASP 对肥大细胞介导的过敏性炎症的有益影响。在体内研究中,我们使用了两种著名的肥大细胞介导的局部和全身过敏性炎症小鼠模型:被动性皮肤过敏性休克(PCA)和主动性全身过敏性休克小鼠模型(ASA)。口服 ASP 可剂量依赖性地抑制免疫球蛋白 (Ig)E 介导的 PCA 反应,表现为埃文斯蓝外渗、耳增厚和肥大细胞脱颗粒。ASP 还能明显减轻卵清蛋白诱导的 ASA 反应,包括低体温、组胺分泌以及 IgE 和白细胞介素-4 的产生。值得注意的是,在抑制过敏性炎症方面,ASP 比罗汉果中另一种抗过敏黄酮类化合物--诺霍法金更为有效。利用肥大细胞系和原代培养肥大细胞(RBL-2H3 和小鼠骨髓源性肥大细胞)阐明了 ASP 对肥大细胞活化的调节机制。ASP 通过抑制 FcεRI 信号通路(Lyn、Fyn 和 Syk)减少了 IgE 刺激的肥大细胞脱颗粒和细胞内钙离子流入。此外,ASP 还通过抑制两种主要转录因子(活化 T 细胞核因子和核因子-κB)来减少促炎细胞因子的表达。综上所述,我们认为 ASP 是治疗肥大细胞介导的过敏性炎症疾病的潜在候选疗法。
Aspalathin, a Primary Rooibos Flavonoid, Alleviates Mast Cell-Mediated Allergic Inflammation by the Inhibition of FcεRI Signaling Pathway.
Mast cells are primary cells initiating allergic inflammation by the release of various allergic mediators, such as histamine and pro-inflammatory cytokines. Aspalathin (ASP) is the predominant flavonoid found exclusively in rooibos, an herb that has been traditionally used in allergy relief therapy. In the present study, we investigated the beneficial effects of ASP on mast cell-mediated allergic inflammation. For in vivo study, two well-known mast cell-mediated local and systemic allergic inflammation mouse models were used: passive cutaneous anaphylaxis (PCA) and active systemic anaphylaxis mouse models (ASA). Oral administration of ASP dose-dependently suppressed immunoglobulin (Ig)E-mediated PCA responses evidenced by Evans blue extravasation, ear thickening, and mast cell degranulation. ASP also significantly mitigated ovalbumin-induced ASA responses, including hypothermia, histamine secretion, and the production of IgE and interleukin-4. Notably, ASP was more effective in suppressing allergic inflammation than nothofagin, another prominent flavonoid known as an anti-allergic component of rooibos. The regulatory mechanism of mast cell activation by ASP was clarified using mast cell line and primary cultured mast cells (RBL-2H3 and mouse bone marrow-derived mast cells). ASP reduced IgE-stimulated mast cells degranulation and intracellular calcium influx by the inhibition of FcεRI signaling pathway (Lyn, Fyn, and Syk). Moreover, ASP reduced pro-inflammatory cytokine expressions by inhibiting two major transcription factors, nuclear factor of activated T cells and nuclear factor-κB. Collectively, we proposed that ASP could be a potential therapeutic candidate for the treatment of mast cell-mediated allergic inflammatory diseases.
期刊介绍:
Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.