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黄豆蔻通过抑制组胺释放和炎性细胞因子产生来抑制肥大细胞介导的过敏反应。

Amomum xanthiodes inhibits mast cell-mediated allergic reactions through the inhibition of histamine release and inflammatory cytokine production.

作者信息

Kim Sang-Hyun, Shin Tae-Yong

机构信息

Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu, South Korea.

出版信息

Exp Biol Med (Maywood). 2005 Oct;230(9):681-7. doi: 10.1177/153537020523000911.

Abstract

In this study, we investigated the effect of Amomum xanthiodes (Zingiberaceae) extract (AXE) on the mast cell-mediated allergy model and studied the possible mechanism of action. We found that AXE inhibited compound 48/80-induced systemic reactions and plasma histamine release in mice. Additionally, AXE decreased immunoglobulin E (IgE)-mediated local allergic reactions and passive cutaneous anaphylaxis (PCA), and AXE dose-dependently attenuated the release of histamine from rat peritoneal mast cells (RPMC) activated by compound 48/80 or IgE. The amounts of AXE needed for inhibition of compound 48/80-induced plasma histamine release and PCA were similar to disodium cromoglycate, the known anti-allergic drug. We found that AXE increased the cAMP levels and decreased the compound 48/80-induced intracellular Ca2+. Furthermore, AXE attenuated the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187)-stimulated tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 secretion in human mast cells. The inhibitory effect of AXE on the proinflammatory cytokines was nuclear factor-kappaB (NF-kappaB)-dependent. In addition, AXE decreased PMA plus A23187-induced degradation of IkappaBalphaand the nuclear translocation of NF-kappaB. Our findings provide evidence that AXE inhibits mast cell-derived immediate-type allergic reactions, and that cAMP, intracellular Ca2+, proinflammatory cytokines, and NF-kappaB are involved in these effects.

摘要

在本研究中,我们研究了黄豆蔻(姜科)提取物(AXE)对肥大细胞介导的过敏模型的影响,并探讨了其可能的作用机制。我们发现AXE可抑制化合物48/80诱导的小鼠全身反应和血浆组胺释放。此外,AXE可减轻免疫球蛋白E(IgE)介导的局部过敏反应和被动皮肤过敏反应(PCA),并且AXE能剂量依赖性地减弱化合物48/80或IgE激活的大鼠腹膜肥大细胞(RPMC)中组胺的释放。抑制化合物48/80诱导的血浆组胺释放和PCA所需的AXE量与已知抗过敏药物色甘酸二钠相似。我们发现AXE可提高环磷酸腺苷(cAMP)水平,并降低化合物48/80诱导的细胞内钙离子(Ca2+)浓度。此外,AXE可减弱佛波酯12-肉豆蔻酸酯13-乙酸酯(PMA)加钙离子载体(A23187)刺激的人肥大细胞中肿瘤坏死因子-α(TNF-α)和白细胞介素(IL)-6的分泌。AXE对促炎细胞因子的抑制作用依赖于核因子-κB(NF-κB)。此外,AXE可减少PMA加A23187诱导的IκBα降解和NF-κB的核转位。我们的研究结果表明,AXE可抑制肥大细胞衍生的速发型过敏反应,并且cAMP、细胞内Ca2+、促炎细胞因子和NF-κB参与了这些作用。

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