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地塞米松抑制臭氧诱导的大鼠肺巨噬细胞炎性蛋白-2的基因表达。

Dexamethasone inhibits ozone-induced gene expression of macrophage inflammatory protein-2 in rat lung.

作者信息

Haddad E B, Salmon M, Sun J, Liu S, Das A, Adcock I, Barnes P J, Chung K F

机构信息

Department of Thoracic Medicine, National Heart & Lung Institute, London, UK.

出版信息

FEBS Lett. 1995 Apr 24;363(3):285-8. doi: 10.1016/0014-5793(95)00333-5.

Abstract

To address the potential role of the chemokine macrophage inflammatory protein-2 (MIP-2) in airway inflammation, we examined whether MIP-2 may play a role in ozone-induced neutrophilic inflammation of airways and its modulation by dexamethasone in rat lung. Following ozone exposure, MIP-2 mRNA expression in the lung peaked at 2 h after exposure and slowly declined thereafter. Dexamethasone suppressed ozone-induced MIP-2 mRNA expression and neutrophil accumulation in the lung. We suggest that the MIP-2 mRNA induction may switch on the neutrophilic influx observed in this model of lung inflammation. Furthermore, the MIP-2 expression is regulated by dexamethasone which may represent one of the mechanisms by which glucocorticoids exert their potent anti-inflammatory properties.

摘要

为了探讨趋化因子巨噬细胞炎性蛋白-2(MIP-2)在气道炎症中的潜在作用,我们研究了MIP-2是否在臭氧诱导的大鼠肺气道嗜中性粒细胞炎症中发挥作用以及地塞米松对其的调节作用。臭氧暴露后,肺中MIP-2 mRNA表达在暴露后2小时达到峰值,随后缓慢下降。地塞米松抑制了臭氧诱导的肺中MIP-2 mRNA表达和嗜中性粒细胞聚集。我们认为,MIP-2 mRNA的诱导可能开启了在该肺部炎症模型中观察到的嗜中性粒细胞流入。此外,MIP-2的表达受地塞米松调节,这可能是糖皮质激素发挥其强大抗炎特性的机制之一。

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