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[脂多糖及抗炎药物对肺血管内巨噬细胞核因子-κB的影响]

[The effects of lipopolysaccharide and anti-inflammatory drugs on nuclear factor-kappa B in pulmonary intravascular macrophage].

作者信息

Cai E, Chen Z, Wu W

机构信息

Institute of Respiratory Medicine of PLA, Xinqiao Hospital, Third Military Medical University, Chongqing 400037.

出版信息

Zhonghua Jie He He Hu Xi Za Zhi. 1999 May;22(5):283-6.

Abstract

OBJECTIVE

To investigate activation of nuclear factor-kappa B(NF-kappa B) in pulmonary intravascular macrophage (PIM) stimulated with lipopolysaccharide (LPS) and effects of anti-inflammatory drugs dexamethasone (DEX) and aspirin (ASA) on the process.

METHODS

PIMs isolated from three healthy pigs were cultured and divided into four groups: Control group; LPS- stimulated group; DEX- or ASA-treated group. The NF-kappa B activity of nuclear protein extract from the PIMs and the concentration of tumor necrosis factor alpha (TNF-alpha) in the supernatant were measured by electrophoretic mobility shift assay (EMSA) and radioimmunoassay (RIA), respectively.

RESULTS

The activity of NF-kappa B significantly increased from 0.5 hr to 4 hr after LPS stimulation (P < 0.01); The level of TNF-alpha in the supernatant elevated markedly from 1 hr to 2 hr after LPS stimulation (P < 0.01); positive correlation was found between the NF-kappa B activity and the TNF-alpha concentration at 1 hr after LPS stimulation (r = 0.991, P < 0.01). Compared with LPS-stimulated group, both NF-kappa B activity and TNF-alpha concentration were significantly lowered in DEX- or ASA-treated groups (P < 0.01).

CONCLUSIONS

LPS might activate NF-kappa B in the PIMs, and induce the increase of transcription and expression of TNF-alpha gene; Both DEX and ASA could inhibit the activation of NF-kappa B and reduce the release of TNF-alpha.

摘要

目的

研究脂多糖(LPS)刺激下肺血管内巨噬细胞(PIM)中核因子-κB(NF-κB)的激活情况,以及抗炎药物地塞米松(DEX)和阿司匹林(ASA)对该过程的影响。

方法

从三头健康猪分离出PIM并进行培养,分为四组:对照组;LPS刺激组;DEX或ASA处理组。分别采用电泳迁移率变动分析(EMSA)和放射免疫分析(RIA)检测PIM核蛋白提取物中NF-κB活性以及上清液中肿瘤坏死因子α(TNF-α)的浓度。

结果

LPS刺激后0.5小时至4小时,NF-κB活性显著增加(P<0.01);LPS刺激后1小时至2小时,上清液中TNF-α水平明显升高(P<0.01);LPS刺激1小时时,NF-κB活性与TNF-α浓度呈正相关(r = 0.991,P<0.01)。与LPS刺激组相比,DEX或ASA处理组的NF-κB活性和TNF-α浓度均显著降低(P<0.01)。

结论

LPS可能激活PIM中的NF-κB,诱导TNF-α基因转录和表达增加;DEX和ASA均可抑制NF-κB的激活并减少TNF-α的释放。

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