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首页|期刊导航|中国药理学通报|地塞米松及N-乙酰半胱氨酸抑制A549细胞IL-8及ICAM-1表达的机制研究

地塞米松及N-乙酰半胱氨酸抑制A549细胞IL-8及ICAM-1表达的机制研究

项琪 付欣 冉丕鑫 张锦 郑西卫 陈娟 郭园园

中国药理学通报Issue(9):1293-1297,1298,6.
中国药理学通报Issue(9):1293-1297,1298,6.DOI:10.3969/j.issn.1001-1978.2014.09.023

地塞米松及N-乙酰半胱氨酸抑制A549细胞IL-8及ICAM-1表达的机制研究

Study of mechanism of DXM and NAC inhibiting expression of IL-8 and ICAM-1 in A549 cells

项琪 1付欣 2冉丕鑫 2张锦 3郑西卫 3陈娟 3郭园园4

作者信息

  • 1. 宁夏医科大学,宁夏 银川 750004
  • 2. 广州医科大学,广东 广州 510182
  • 3. 宁夏医科大学总医院呼吸与危重症医学科,宁夏 银川 750004
  • 4. 大庆市第四医院,黑龙江 大庆 163712
  • 折叠

摘要

Abstract

Aim To study the mechanism of DXM and NAC inhibiting the expression of IL-8 and ICAM-1 in A549 cells. Methods The expression of IL-8 and ICAM-1 was detected by ELISA and flow cytometry re-spectively; the expression of GR,HDAC,AP-1,NF-κB was detected by Western blot, while the activity of HDAC was detected by spectrophotometry. ResultsThe increasing expression of IL-8 and ICAM-1 induced by TNF-α could be inhibited by DXM and NAC in A549 cells. DXM could inhibit the transcribed activa-tion of AP-1,NF-κB, and the expression of HDAC and its activity induced by TNF-α and LPS; NAC only in-hibited the transcribed activation of NF-κB, while it had no affection on the transcribed activation of AP-1 and the expression of HDAC and its activity. Conclu-sions DXM and NAC both have the anti-inflammatory effect. DXM plays the role of anti-inflammation through increasing the expression and activation of HDAC, in-hibiting the transcribed activation of AP-1 and NF-κB, while NAC has no effect on the expression and activa-tion of HDAC, which shows that NAC does not exert anti-inflammatory effect through acetylation signal.

关键词

肺疾病/慢性阻塞性/炎症反应/地塞米松/N-乙酰半胱氨酸/乙酰化信号

Key words

pulmonary disease/chronic obstructive/the inflammatory response/dexamethasone/N-acetyl cyste-ine/acetylation signal

引用本文复制引用

项琪,付欣,冉丕鑫,张锦,郑西卫,陈娟,郭园园..地塞米松及N-乙酰半胱氨酸抑制A549细胞IL-8及ICAM-1表达的机制研究[J].中国药理学通报,2014,(9):1293-1297,1298,6.

基金项目

国家自然科学基金青年基金项目( No 30800501) ( No 30800501)

宁夏自然科学基金资助项目(No NZ11278) (No NZ11278)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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