Effects of dexamethasone and ibuprofen on LPS-induced gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung

被引:0
|
作者
Qiu, HB [1 ]
Pan, JQ [1 ]
Zhao, YQ [1 ]
Chen, DC [1 ]
机构
[1] CHINESE ACAD SCI,PEKING UNION MED COLL HOSP,DEPT HEMATOL,BEIJING 100730,PEOPLES R CHINA
来源
ACTA PHARMACOLOGICA SINICA | 1997年 / 18卷 / 02期
关键词
Wistar rats; lipopolysaccharides; tumor necrosis factor; interleukin-1; gene expression; dexamethasone; ibuprofen; respiratory distress syndrome;
D O I
暂无
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
AIM: To study the kinetics of tumor necrosis factor alpha (TNF alpha), interleukin-1 beta (IL-1 beta), and macrophage inflammatory protein-1 alpha (MIP-1 alpha) gene expression in rat lung after ip lipopolysaccharides (LPS) and the effect of dexamethasone (Dex) and ibuprofen (Ibu) on the cytokines gene expression. METHODS: The amount of Evans blue in lung was measured by fluorescence method. The mRNA levels of TNF alpha, IL-1 beta and MIP-1 alpha in rat lung were assessed by slot blot analysis. RESULTS: The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung after ip LPS increased in a dose-dependent manner, and peaked at 2, 6, and 12 h, respectively. Both Dex 50 mg . kg(-1) and Ibu 90 mg . kg(-1) injected at 1 h before ip LPS markedly decreased the content of Evans blue in lung at 1 h after ip LPS. After Dex or Ibu pretreatment, the peak levels of TNF alpha, IL-1 beta, and MIP-1 alpha mRNA decreased markedly compared with LPS alone. CONCLUSION: The gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung increased after ip LPS. Dex and Ibu prevented LPS-induced lung injury through inhibiting the cytokines gene expression.
引用
收藏
页码:165 / 168
页数:4
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