Inhibitory effect of methyleugenol on IgE-mediated allergic inflammation in RBL-2H3 cells.

Inhibitory effect of methyleugenol on IgE-mediated allergic inflammation in RBL-2H3 cells.
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甲基丁香酚对 RBL-2H3 细胞 IgE 介导的过敏性炎症的抑制作用

DOI:
10.1155/2015/463530
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发表时间:
2015
影响因子:
4.6
通讯作者:
Tan X
Tan X
中科院分区:
医学3区
文献类型:
--
作者:
Tang F;Chen F;Ling X;Huang Y;Zheng X;Tang Q;Tan X

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过敏性疾病,如哮喘和过敏性鼻炎,是常见的。因此,发现治疗这些疾病的药物是必不可少的。甲基丁香酚(ME)是一种天然化合物,具有抗过敏、抗过敏、抗伤害和抗炎作用。本研究探讨了ME对IgE介导的炎症反应的抗过敏作用及其在肥大细胞系RBL-2 H3中的抗过敏机制。我们发现ME显著抑制β-氨基己糖苷酶、肿瘤坏死因子-(TNF-)α和白细胞介素-(IL-)4的释放,并且在测试浓度(0-100 μM)下没有细胞毒性。此外,ME显著减少促炎脂质介质前列腺素E2(PGE 2)、前列腺素D2(PGD 2)、白三烯B4(LTB 4)和白三烯C4(LTC 4)的产生。我们进一步评估了ME对FcεRI级联反应早期阶段的影响。ME显著抑制Syk磷酸化和表达,但对林恩无影响。此外,它抑制ERK 1/2、p38和JNK磷酸化,这与促炎细胞因子表达有关。ME还降低胞浆磷脂酶A2(cPLA 2)和5-脂氧合酶(5-LO)磷酸化以及环氧化酶-2(考克斯-2)表达。这些结果表明,ME通过抑制Syk、ERK 1/2、p38、JNK、cPLA 2和5-LO的活化来抑制过敏反应。ME对考克斯-2表达的抑制作用可能与其抗过敏作用有关。
Allergic diseases, such as asthma and allergic rhinitis, are common. Therefore, the discovery of therapeutic drugs for these conditions is essential. Methyleugenol (ME) is a natural compound with antiallergic, antianaphylactic, antinociceptive, and anti-inflammatory effects. This study examined the antiallergic effect of ME on IgE-mediated inflammatory responses and its antiallergy mechanism in the mast cell line, RBL-2H3. We found that ME significantly inhibited the release of β-hexosaminidase, tumor necrosis factor- (TNF-) α, and interleukin- (IL-) 4, and was not cytotoxic at the tested concentrations (0–100 μM). Additionally, ME markedly reduced the production of the proinflammatory lipid mediators prostaglandin E2 (PGE2), prostaglandin D2 (PGD2), leukotriene B4 (LTB4), and leukotriene C4 (LTC4). We further evaluated the effect of ME on the early stages of the FcεRI cascade. ME significantly inhibited Syk phosphorylation and expression but had no effect on Lyn. Furthermore, it suppressed ERK1/2, p38, and JNK phosphorylation, which is implicated in proinflammatory cytokine expression. ME also decreased cytosolic phospholipase A2 (cPLA2) and 5-lipoxygenase (5-LO) phosphorylation and cyclooxygenase-2 (COX-2) expression. These results suggest that ME inhibits allergic response by suppressing the activation of Syk, ERK1/2, p38, JNK, cPLA2, and 5-LO. Furthermore, the strong inhibition of COX-2 expression may also contribute to the antiallergic action of ME. Our study provides further information about the biological functions of ME.
DOI: 10.3904/kjim.2011.26.1.8
发表时间: 2011-03
期刊: The Korean journal of internal medicine
影响因子: --
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