Sesamin attenuates mast cell-mediated allergic responses by suppressing the activation of p38 and nuclear factor-κB
Sesamin attenuates mast cell-mediated allergic responses by suppressing the activation of p38 and nuclear factor-κB
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芝麻素通过抑制 p38 和核因子-κB 的激活来减弱肥大细胞介导的过敏反应
DOI：
10.3892/mmr.2015.4546
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发表时间：
2016-01-01
影响因子：
3.4
通讯作者：
Yan, Guang Hai
中科院分区：
文献类型：
--
作者：
Li, Liang Chang;Piao, Hong Mei;Yan, Guang Hai
建立治疗变态反应性疾病的药物是人类健康研究的重要焦点。芝麻素是芝麻油中的一种木脂素，具有多种药理作用。然而，据我们所知，芝麻素对肥大细胞介导的过敏反应的影响尚未被研究。因此，本研究的目的是探讨芝麻素对肥大细胞介导的过敏反应的影响及其产生这种作用的潜在机制。在大鼠中，口服芝麻素可抑制被动皮肤过敏反应。芝麻素可抑制免疫球蛋白E诱导的大鼠腹膜肥大细胞组胺释放，其机制可能与细胞内钙调节有关。在人类肥大细胞中，芝麻素降低了佛波酯12-肉豆蔻酸酯13-乙酸酯和钙离子载体A23187对促炎细胞因子的产生和分泌的刺激作用，包括肿瘤坏死因子-a和白介素6。芝麻素对促炎症细胞因子产生的抑制作用依赖于活化B细胞核因子X轻链增强子B和p38丝裂原活化蛋白激酶。目前的研究表明，芝麻素通过阻断组胺的释放，以及促炎细胞因子的产生和分泌来抑制肥大细胞来源的炎性过敏反应。此外，研究结果表明，芝麻素的作用是通过其对p38MAPK/NF-kappa B信号通路的影响而实现的。此外，本研究报道的芝麻素在体内和体外的抗过敏作用表明，它是一种有前途的炎症性变态反应性疾病的治疗剂。
Establishing therapeutic agents for the treatment of allergic diseases is an important focus of human health research. Sesamin, a lignan in sesame oil, exhibits a diverse range of pharmacological properties. However, to the best of our knowledge, the effect of sesamin on mast cell-mediated allergic responses has not yet been investigated. Thus, the aim of the present study was to investigate the effect of sesamin on mast cell-mediated allergic responses and the underlying mechanisms by which it produces this effect. In rats, oral administration of sesamin inhibited passive cutaneous anaphylaxis. Sesamin exposure attenuated immunoglobulin E-induced histamine release from rat peritoneal mast cells, which was indicated to be mediated by the modulation of intracellular calcium. In human mast cells, sesamin reduced the stimulatory effects of phorbol 12-myristate 13-acetate and calcium ionophore A23187 on the production and secretion of pro-inflammatory cytokines, including tumor necrosis factor-a and interleukin-6. The inhibitory effect of sesamin on pro-inflammatory cytokine production was dependent on nuclear factor x-light-chain-enhancer of activated B cells (NF-kappa B) and p38 mitogen-activated protein kinase (MAPK). The present study demonstrates that sesamin inhibits mast cell-derived inflammatory allergic reactions by blocking histamine release, and pro-inflammatory cytokine production and secretion. In addition, the findings indicate that the effect of sesamin is mediated by its effect on p38 MAPK/NF-kappa B signaling. Furthermore, the in vivo and in vitro anti-allergic effects of sesamin reported in the present study suggest that it is a promising therapeutic agent for the treatment of inflammatory allergic diseases.