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超氧化溶液可抑制肥大细胞中IgE抗原诱导的脱颗粒和细胞因子释放。

Super-oxidized solution inhibits IgE-antigen-induced degranulation and cytokine release in mast cells.

作者信息

Medina-Tamayo J, Sánchez-Miranda E, Balleza-Tapia H, Ambriz X, Cid M E, González-Espinosa D, Gutiérrez A A, González-Espinosa C

机构信息

Pharmacobiology Department, Cinvestav, South Campus, Mexico City, Mexico.

出版信息

Int Immunopharmacol. 2007 Aug;7(8):1013-24. doi: 10.1016/j.intimp.2007.03.005. Epub 2007 Apr 16.

Abstract

Activation of the high affinity IgE receptor (Fc epsilonRI) through IgE-antigen complexes induces mast cell degranulation, synthesis of lipid mediators and cytokine production. These effects are involved in Type I hypersensitivity reactions and controlling them has been the main objective of many anti-allergic therapies. Here we report that pretreatment of murine bone marrow derived mast cells (BMMC) with super-oxidized solution (SOS) inhibits Fc epsilonRI dependent-beta hexosaminidase and cytokine release. This effect is exerted without altering total protein tyrosine phosphorylation, MAPK activation, cytokine mRNA accumulation or calcium mobilization after Fc epsilonRI triggering. Our data suggest that this neutral pH-SOS acts like a mast cell-membrane stabilizer inhibiting the cell machinery for granule secretion without altering the signal transduction pathways induced by IgE-antigen receptor crosslinking.

摘要

通过IgE-抗原复合物激活高亲和力IgE受体(FcεRI)可诱导肥大细胞脱颗粒、脂质介质合成和细胞因子产生。这些效应参与I型超敏反应,而控制这些反应一直是许多抗过敏疗法的主要目标。在此我们报告,用超氧化溶液(SOS)预处理小鼠骨髓来源的肥大细胞(BMMC)可抑制FcεRI依赖性β-己糖胺酶和细胞因子释放。在FcεRI触发后,这种效应的发挥不会改变总蛋白酪氨酸磷酸化、MAPK激活、细胞因子mRNA积累或钙动员。我们的数据表明,这种中性pH值的SOS就像一种肥大细胞膜稳定剂,可抑制颗粒分泌的细胞机制,而不会改变由IgE-抗原受体交联诱导的信号转导途径。

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