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地塞米松和布洛芬对脂多糖诱导的大鼠肺组织中肿瘤坏死因子α、白细胞介素-1β和巨噬细胞炎性蛋白-1α基因表达的影响。

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

作者信息

Qiu H B, Pan J Q, Zhao Y Q, Chen D C

机构信息

Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.

出版信息

Zhongguo Yao Li Xue Bao. 1997 Mar;18(2):165-8.

Abstract

AIM

To study the kinetics of tumor necrosis factor alpha (TNF alpha), interleukine-1 (IL-1 beta), and macrophage inflammatory protein-1 alpha (MIP-1 alpha) gene expression in rat lung after i.p. 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 i.p. 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 i.p. LPS markedly decreased the content of Evans blue in lung at 1 h after i.p. 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 i.p. LPS. Dex and Ibu prevented LPS-induced lung injury through inhibiting the cytokines gene expression.

摘要

目的

研究腹腔注射脂多糖(LPS)后大鼠肺组织中肿瘤坏死因子α(TNFα)、白细胞介素-1(IL-1β)和巨噬细胞炎性蛋白-1α(MIP-1α)基因表达的动力学,以及地塞米松(Dex)和布洛芬(Ibu)对细胞因子基因表达的影响。

方法

采用荧光法测定肺组织中伊文思蓝的含量。通过狭缝印迹分析评估大鼠肺组织中TNFα、IL-1β和MIP-1α的mRNA水平。

结果

腹腔注射LPS后,大鼠肺组织中TNFα、IL-1β和MIP-1α的mRNA水平呈剂量依赖性增加,分别在2、6和12小时达到峰值。在腹腔注射LPS前1小时注射50mg·kg-1的Dex和90mg·kg-1的Ibu,均可显著降低腹腔注射LPS后1小时肺组织中伊文思蓝的含量。与单独使用LPS相比,Dex或Ibu预处理后,TNFα、IL-1β和MIP-1α mRNA的峰值水平显著降低。

结论

腹腔注射LPS后大鼠肺组织中TNFα、IL-1β和MIP-1α的基因表达增加。Dex和Ibu通过抑制细胞因子基因表达预防LPS诱导的肺损伤。

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