Kim Min-Ah, Lee Jin-Ho, Woo Keunjung, Jeong Eunwoo, Kim Tack-Joong
Division of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of Korea.
Research & Development Center, Doctor TJ Co., Ltd., Wonju 26493, Republic of Korea.
Biomedicines. 2025 Jun 25;13(7):1547. doi: 10.3390/biomedicines13071547.
: Allergens can trigger severe immune responses in hypersensitive individuals, with mast cells releasing inflammatory mediators via IgE-FcɛRI signaling. Spleen tyrosine kinase (Syk) is a key regulator in this pathway, making it a promising therapeutic target. Natural modulators of Syk-mediated mast cell activation remain underexplored. This study investigated the anti-allergic effects of a 70% ethanol extract of (SME) using in vitro and in vivo models. : SME was evaluated using IgE-sensitized RBL-2H3 cells, a passive cutaneous anaphylaxis model, and a DNCB-induced atopic dermatitis-like mouse model. Allergic responses were assessed via degranulation assays, histopathology, serum IgE levels, and the spleen index. : SME significantly inhibited mast cell degranulation by 44.4 ± 1.6% in RBL-2H3 cells at 100 µg/mL following 30 min of treatment compared to the untreated control. Western blot analysis demonstrated dose-dependent suppression of protein kinase B (PKB, also known as AKT), c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and spleen tyrosine kinase (Syk) phosphorylation, indicating inhibition of key allergic signaling pathways. In an IgE/Ag-induced passive cutaneous anaphylaxis model in ICR mice, SME (100 mg/kg, orally) significantly attenuated vascular permeability, as evidenced by a 20.6 ± 9.7% reduction in Evans blue extravasation relative to the Ag-treated group. In a 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis (AD)-like model, six treatments of SME significantly improved the skin condition, reduced spleen enlargement associated with allergic inflammation, and decreased serum IgE levels by 43.3 ± 11.2% compared to the DNCB group. : These findings suggest that SME may help to alleviate allergic responses and AD by modulating key immune signaling pathways.
过敏原可在过敏个体中引发严重的免疫反应，肥大细胞通过IgE-FcɛRI信号释放炎症介质。脾酪氨酸激酶（Syk）是该途径中的关键调节因子，使其成为一个有前景的治疗靶点。Syk介导的肥大细胞活化的天然调节剂仍未得到充分研究。本研究使用体外和体内模型研究了[植物名称]70%乙醇提取物（SME）的抗过敏作用。：使用IgE致敏的RBL-2H3细胞、被动皮肤过敏反应模型和二硝基氯苯（DNCB）诱导的特应性皮炎样小鼠模型对SME进行评估。通过脱颗粒试验、组织病理学、血清IgE水平和脾脏指数评估过敏反应。：与未处理的对照组相比，在100μg/mL浓度下处理30分钟后，SME在RBL-2H3细胞中显著抑制肥大细胞脱颗粒44.4±1.6%。蛋白质印迹分析表明，蛋白激酶B（PKB，也称为AKT）、c-Jun氨基末端激酶（JNK）、细胞外信号调节激酶（ERK）和脾酪氨酸激酶（Syk）的磷酸化呈剂量依赖性抑制，表明关键的过敏信号通路受到抑制。在ICR小鼠的IgE/抗原诱导的被动皮肤过敏反应模型中，SME（100mg/kg，口服）显著减轻血管通透性，相对于抗原处理组，伊文思蓝外渗减少20.6±9.7%证明了这一点。在1-氯-2,4-二硝基苯（DNCB）诱导的特应性皮炎（AD）样模型中，六次给予SME显著改善了皮肤状况，减少了与过敏性炎症相关的脾脏肿大，与DNCB组相比，血清IgE水平降低了43.3±11.2%。：这些发现表明，SME可能通过调节关键免疫信号通路来帮助减轻过敏反应和AD。
