首页> 美国卫生研究院文献>Biomolecules Therapeutics >Curcumin Inhibits the Activation of Immunoglobulin E-Mediated Mast Cells and Passive Systemic Anaphylaxis in Mice by Reducing Serum Eicosanoid and Histamine Levels
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Curcumin Inhibits the Activation of Immunoglobulin E-Mediated Mast Cells and Passive Systemic Anaphylaxis in Mice by Reducing Serum Eicosanoid and Histamine Levels

机译:姜黄素通过降低血清类花生酸和组胺水平抑制小鼠免疫球蛋白E介导的肥大细胞的活化和被动全身性过敏反应

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摘要

Curcumin is naturally occurring polyphenolic compound found in turmeric and has many pharmacological activities. The present study was undertaken to evaluate anti-allergic inflammatory activity of curcumin, and to investigate its inhibitory mechanisms in immunoglobulin E (IgE)/Ag-induced mouse bone marrow-derived mast cells (BMMCs) and in a mouse model of IgE/Ag-mediated passive systemic anaphylaxis (PSA). Curcumin inhibited cyclooxygenase-2 (COX-2) dependent prostaglandin D2 (PGD2) and 5-lipoxygenase (5-LO) dependent leukotriene C4 (LTC4) generation dose-dependently in BMMCs. To probe the mechanism involved, we assessed the effects of curcumin on the phosphorylation of Syk and its downstream signal molecules. Curcumin inhibited intracellular Ca2+ influx via phospholipase Cγ1 (PLCγ1) activation and the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor-κB (NF-κB) pathway. Furthermore, the oral administration of curcumin significantly attenuated IgE/Ag-induced PSA, as determined by serum LTC4, PGD2, and histamine levels. Taken together, this study shows that curcumin offers a basis for drug development for the treatment of allergic inflammatory diseases.
机译:姜黄素是姜黄中天然存在的多酚化合物,具有许多药理活性。进行本研究以评估姜黄素的抗过敏炎症活性,并研究其在免疫球蛋白E(IgE)/ Ag诱导的小鼠骨髓源性肥大细胞(BMMC)和IgE / Ag小鼠模型中的抑制机制介导的被动全身过敏反应(PSA)。姜黄素抑制BMMCs中环加氧酶2(COX-2)依赖性前列腺素D2(PGD2)和5-脂加氧酶(5-LO)依赖性白三烯C4(LTC4)的产生。为了探究涉及的机制,我们评估了姜黄素对Syk及其下游信号分子磷酸化的影响。姜黄素通过磷脂酶Cγ1(PLCγ1)活化,丝裂原活化蛋白激酶(MAPKs)和核因子-κB(NF-κB)途径的磷酸化抑制细胞内Ca 2 + 流入。此外,口服姜黄素可显着减弱IgE / Ag诱导的PSA,如血清LTC4,PGD2和组胺水平所确定。两者合计,这项研究表明姜黄素为治疗过敏性炎症疾病的药物开发提供了基础。

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