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蜂毒对肥大细胞介导的过敏炎症反应的抑制作用。

Inhibitory effects of bee venom on mast cell-mediated allergic inflammatory responses.

机构信息

Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju, Gangwon‑do 26339, Republic of Korea.

Catholic Precision Medicine Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.

出版信息

Int J Mol Med. 2018 Jun;41(6):3717-3726. doi: 10.3892/ijmm.2018.3558. Epub 2018 Mar 12.

DOI:10.3892/ijmm.2018.3558
PMID:29532852
Abstract

Although bee venom (BV) is a toxin that causes bee stings to be painful, it has been widely used clinically for the treatment of certain immune‑associated diseases. BV has been used traditionally for the treatment of chronic inflammatory diseases. In this regard, the present study analyzed the effect of BV on the regulation of inflammatory mediator production by mast cells and their allergic inflammatory responses in an animal model. HMC‑1 cells were treated with BV prior to stimulation with phorbol‑12‑myristate 13‑acetate plus calcium ionophore A23187 (PMACI). The production of allergy‑associated pro‑inflammatory mediators was examined, and the underlying mechanisms were investigated. Furthermore, to investigate whether BV exhibits anti‑inflammatory effects associated with anti‑allergic effects in vivo, a compound 48/80‑induced anaphylaxis model was used. BV inhibited histamine release, mRNA expression and production of cytokines in the PMACI‑stimulated HMC‑1 cells. Furthermore, the inhibitory effects of BV on mitogen‑activated protein kinase (MAPK), MAPK kinase, signal transducer and activator of transcription 3 (STAT3) and Akt were demonstrated. The present study also investigated the ability of BV to inhibit compound 48/80‑induced systemic anaphylaxis in vivo. BV protected the mice against compound 48/80‑induced anaphylactic‑associated mortality. Furthermore, BV suppressed the mRNA expression levels of pro‑inflammatory cytokines, and suppressed the activation of MAPK and STAT3 in this model. These results provide novel insights into the possible role of BV as a modulator for mast cell‑mediated allergic inflammatory disorders.

摘要

虽然蜂毒(BV)是一种导致蜜蜂蜇伤疼痛的毒素,但它已被广泛应用于某些与免疫相关疾病的临床治疗。传统上,BV 已被用于治疗慢性炎症性疾病。在这方面,本研究分析了 BV 对肥大细胞炎症介质产生的调节作用及其在动物模型中的过敏炎症反应。在刺激佛波醇 12-肉豆蔻酸 13-醋酸盐加钙离子载体 A23187(PMACI)之前,用 BV 处理 HMC-1 细胞。检测过敏相关促炎介质的产生,并探讨其潜在机制。此外,为了研究 BV 是否在体内表现出与抗过敏作用相关的抗炎作用,使用了化合物 48/80 诱导的过敏反应模型。BV 抑制 PMACI 刺激的 HMC-1 细胞中组胺释放、mRNA 表达和细胞因子产生。此外,还证明了 BV 对丝裂原激活的蛋白激酶(MAPK)、MAPK 激酶、信号转导和转录激活因子 3(STAT3)和 Akt 的抑制作用。本研究还研究了 BV 在体内抑制化合物 48/80 诱导的全身性过敏反应的能力。BV 保护小鼠免受化合物 48/80 诱导的过敏相关死亡率。此外,BV 抑制了该模型中促炎细胞因子的 mRNA 表达水平,并抑制了 MAPK 和 STAT3 的激活。这些结果为 BV 作为肥大细胞介导的过敏炎症性疾病调节剂的可能作用提供了新的见解。

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