DEXAMETHASONE INHIBITS OZONE-INDUCED GENE-EXPRESSION OF MACROPHAGE INFLAMMATORY PROTEIN-2 IN RAT LUNG

被引：26

作者：

HADDAD, EB ^{[1
]}

SALMON, M ^{[1
]}

SUN, J ^{[1
]}

LIU, S ^{[1
]}

DAS, A ^{[1
]}

ADCOCK, I ^{[1
]}

BARNES, PJ ^{[1
]}

CHUNG, KF ^{[1
]}

机构：

[1] NATL HEART & LUNG INST,DEPT THORAC MED,LONDON SW3 6LY,ENGLAND

来源：

FEBS LETTERS | 1995年 / 363卷 / 03期

基金：

英国医学研究理事会;

关键词：

OZONE; RAT LUNG; INFLAMMATION; NORTHERN BLOT; MIP-2; MESSENGER-RNA; DEXAMETHASONE;

D O I：

10.1016/0014-5793(95)00333-5

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：285 / 288

页数：4

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