深海来源的丁内酯 I 通过调节肥大细胞功能抑制卵清蛋白诱导的过敏反应在小鼠模型中。
Deep-Sea-Derived Butyrolactone I Suppresses Ovalbumin-Induced Anaphylaxis by Regulating Mast Cell Function in a Murine Model.
机构信息
College of Food and Biological Engineering, Xiamen Key Laboratory of Marine Functional Food, Fujian Provincial Engineering Technology Research Center of Marine Functional Food, Fujian Collaborative Innovation Center for Exploitation and Utilization of Marine Biological Resources , Jimei University , 43 Yindou Road , Xiamen , 361021 Fujian , P.R. China.
Key Laboratory of Marine Biogenetic Resources, South China Sea Bio-Resource Exploitation and Utilization Collaborative Innovation Center , Third Institute of Oceanography, State Oceanic Administration , 184 Daxue Road , Xiamen , 361005 Fujian , P.R. China.
出版信息
J Agric Food Chem. 2018 Jun 6;66(22):5581-5592. doi: 10.1021/acs.jafc.8b01674. Epub 2018 May 22.
Deep-sea-derived butyrolactone I (BTL-I), which was identified as a type of butanolide, was isolated from Aspergillus sp. Ovalbumin (OVA)-induced BALB/c anaphylaxis was established to explore the antifood allergic activity of BTL-I. As a result, BTL-I was able to alleviate OVA-induced allergy symptoms, reduce the levels of histamine and mouse mast cell proteinases, inhibit OVA-specific IgE, and decrease the population of mast cells in the spleen and mesenteric lymph nodes. BTL-I also significantly suppressed mast-dependent passive cutaneous anaphylaxis. Additionally, the maturation of bone marrow-derived mast cells (BMMCs) declined as BTL-I caused down-regulation of c-KIT receptors. Furthermore, molecular docking analyses revealed that BTL-I interacted with the inhibitory receptor, FcγRIIB. In conclusion, the reduction of mast cell function by deep-sea-derived BTL-I as well as its interactions with the inhibitory receptor, FcγRIIB, may contribute to BTL-I-related protection against food anaphylaxis.
深海来源的丁内酯 I（BTL-I）被鉴定为一种丁内酯，从曲霉菌属中分离出来。卵清蛋白（OVA）诱导的 BALB/c 过敏反应被建立，以探索 BTL-I 的抗食物过敏活性。结果表明，BTL-I 能够缓解 OVA 诱导的过敏症状，降低组氨酸和鼠肥大细胞蛋白酶的水平，抑制 OVA 特异性 IgE，并减少脾脏和肠系膜淋巴结中的肥大细胞数量。BTL-I 还显著抑制了肥大细胞依赖性被动皮肤过敏反应。此外，骨髓来源的肥大细胞（BMMC）的成熟因 BTL-I 引起 c-KIT 受体下调而下降。此外，分子对接分析表明，BTL-I 与抑制性受体 FcγRIIB 相互作用。总之，深海来源的 BTL-I 通过降低肥大细胞功能及其与抑制性受体 FcγRIIB 的相互作用可能有助于 BTL-I 相关的食物过敏保护。
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