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在接受角叉菜胶诱导性胸膜炎的对照大鼠和饮酒大鼠中，NF-κB/RelA-p50及NF-κB/p50-p50的差异性激活

Differential activation of NF kappa B/RelA-p50 and NF kappa B/p50-p50 in control and alcohol-drinking rats subjected to carrageenin-induced pleurisy.

作者信息

Singh Ashok K, Jiang Yin

机构信息

Department of Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota, St Paul Campus, St Paul, MN 55108, USA.

出版信息

Mediators Inflamm. 2004 Aug;13(4):255-62. doi: 10.1080/09629350400003035.

DOI:10.1080/09629350400003035

PMID:15545056

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1781568/

Abstract

BACKGROUND

Carrageenin (CAR) injection into the pleural cavity causes local inflammation called carrageenin-induced pleurisy (CAR-IP). Inflammation onset is characterized by an activation of pro-inflammatory NFkappaB, RelA-p50, while inflammation resolution is characterized by an activation of an anti-inflammatory NFkappaB, p50-p50, that re-establishes homeostasis, an essential process for an organism's survival. Although chronic alcohol intake disrupts inflammation, the mechanism behind the development of inflammatory disorder in alcoholics is not yet known. Therefore, the aim of this investigation was to study the effects of ethanol intake on CAR-IP and NFkappaB activation in pleural fluid neutrophils in P rats.

METHODS

Alcohol-preferring, P rats were given free choice of alcohol (15% ethanol) and water or water alone (for control) for 15 days. Then, each rat was injected with 0.2 ml of 2% CAR into the pleural cavity under light ether anesthesia. At different time intervals after the CAR injection, rats were anesthetized and their blood and pleural fluid samples were collected. Pleural fluid inflammatory cells were identified with Turk's or Wright-Giemsa staining. Different cell types were sorted using a fluorescence-activated cell sorter. Pleural fluid neutrophils were examined for apoptosis and activation of the two NFkappaB subspecies.

RESULTS

In control rats, fluid began to accumulate in the pleural cavity 0.5 h after, which peaked 24 h after, CAR injection. Then, the values declined gradually. The increase in pleural fluid correlated with RelA-p50 activation, while the decline in pleural fluid correlated with p50-p50 activation and apoptosis in neutrophils. In alcohol-drinking rats, pleural fluid remained elevated for up to 6 days after CAR injection. Neutrophils from alcohol-drinking rats exhibited suppressed apoptosis, augmented RelA-p50 activation, and suppressed p50-p50 activation.

CONCLUSIONS

Alcohol intake prolonged inflammation in P rats. An alcohol-induced upregulation of RelA-p50 activation and downregulation of p50-p50 activation may be causally related to the alcohol-induced inflammation dysregulation.

摘要

背景

向胸腔内注射角叉菜胶（CAR）会引发局部炎症，称为角叉菜胶诱导的胸膜炎（CAR-IP）。炎症发作的特征是促炎核因子κB（NFκB）、RelA-p50的激活，而炎症消退的特征是抗炎NFκB、p50-p50的激活，其重新建立内环境稳态，这是生物体生存的必要过程。尽管长期饮酒会扰乱炎症反应，但酗酒者炎症性疾病发生背后的机制尚不清楚。因此，本研究的目的是探讨乙醇摄入对P大鼠角叉菜胶诱导胸膜炎（CAR-IP）及胸腔积液中性粒细胞中NFκB激活的影响。

方法

将嗜酒的P大鼠自由选择酒精（15%乙醇）和水或仅给予水（作为对照），持续15天。然后，在轻度乙醚麻醉下，向每只大鼠胸腔内注射0.2 ml 2%的角叉菜胶。在注射角叉菜胶后的不同时间间隔，将大鼠麻醉并采集其血液和胸腔积液样本。用 Türk 或 Wright-Giemsa 染色鉴定胸腔积液中的炎性细胞。使用荧光激活细胞分选仪对不同细胞类型进行分选。检测胸腔积液中性粒细胞的凋亡及两种NFκB亚型的激活情况。

结果

在对照大鼠中，胸腔积液在注射角叉菜胶后0.5小时开始积聚，24小时达到峰值。然后，数值逐渐下降。胸腔积液的增加与RelA-p50激活相关，而胸腔积液的减少与p50-p50激活及中性粒细胞凋亡相关。在饮酒大鼠中，注射角叉菜胶后胸腔积液在长达6天内持续升高。饮酒大鼠的中性粒细胞表现出凋亡受抑制、RelA-p50激活增强及p50-p50激活受抑制。