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首页> 外文期刊>Journal of immunotoxicology. >Amaranthus spinosus Linn. Inhibits mast cell-mediated anaphylactic reactions
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Amaranthus spinosus Linn. Inhibits mast cell-mediated anaphylactic reactions

机译：mar菜Linn。抑制肥大细胞介导的过敏反应

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摘要

The current study characterizes the mechanism by which the Amaranthus spinosus (Amaranthaceae) decreases mast cell-mediated anaphylactic reactions. Anaphylaxis is a typical hypersensitivity Type I reaction, sharing common mechanisms with asthma in its early and late phases. Mast cells are key as effector cells in hypersensitivity Type I reactions. A. spinosus has been traditionally used in the treatment of allergic bronchitis and asthma, but its role in mast cell-mediated anaphylactic reactions has not fully been investigated. This report investigated the potential effects of the ethyl acetate fraction of A. spinosus leaves (EAFAS) against a Compound 48/80 (potent secretagogue)-induced systemic anaphylactic shock paradigm in a mouse model. In addition, rat peritoneal mast cells (RPMC) were used in in vitro studies to investigate the effect of EAFAS on Compound 48/80-induced peritoneal mast cell degranulation and histamine release. When administration by the oral route1h before Compound 48/80 injectionEAFAS (at dose from 0.0011g/kg) completely inhibited the induced anaphylactic shock. EAFAS at concentrations ranging 0.251mg/ml dose-dependently attenuated rates of mast cell degranulation and histamine release from RPMC that were evoked by Compound 48/80. The results of the present investigation indicated that EAFAS stabilizes the mast cell lipid bilayer membrane, thereby preventing the perturbation of membrane and the release of histamine. As a result of these anti-degranulating and anti-histaminic effects, it can be suggested that EAFAS may have a potential use in the prophylaxis and management of anaphylactic reactions.
机译：当前的研究表征了spin菜（A菜）减少肥大细胞介导的过敏反应的机制。过敏反应是典型的I型超敏反应，在哮喘的早期和晚期具有共同的机制。肥大细胞是I型超敏反应中效应细胞的关键。传统上将棘孢曲霉用于治疗变应性支气管炎和哮喘，但是尚未完全研究其在肥大细胞介导的过敏反应中的作用。这份报告调查了小鼠模型中棘孢曲霉（AFA）的乙酸乙酯级分（EAFAS）对化合物48/80（强促分泌素）诱导的系统性过敏性休克范例的潜在影响。另外，在体外研究中使用了大鼠腹膜肥大细胞（RPMC）来研究EAFAS对化合物48/80诱导的腹膜肥大细胞脱粒和组胺释放的影响。在化合物48/80注射前1小时通过口服途径给药时，EAFAS（剂量为0.0011g / kg）完全抑制了诱发的过敏性休克。浓度为0.251mg / ml的EAFAS剂量依赖性地减弱了化合物48/80引起的肥大细胞脱粒和RPMC组胺释放的速率。本研究的结果表明，EAFAS稳定了肥大细胞脂质双层膜，从而防止了膜的扰动和组胺的释放。这些抗脱粒和抗组胺作用的结果表明，EAFAS在预防和处理过敏反应方面可能具有潜在用途。

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