炎症细胞模型中肠上皮细胞核因子-κB的调控
Regulation of nuclear factor-kappaB in intestinal epithelial cells in a cell model of inflammation.
作者信息
Homaidan Fadia R, Chakroun Iman, El-Sabban Marwan E
机构信息
Department of Physiology, American University of Beirut, Faculty of Medicine, Beirut, Lebanon.
出版信息
Mediators Inflamm. 2003 Oct;12(5):277-83. doi: 10.1080/09629350310001619681.
Abstract
BACKGROUND
Interleukin-1 (IL-1), an inflammatory cytokine whose levels are elevated in inflamed mucosa, causes part of its effect on intestinal epithelial cells (IEC) through inducing ceramide production.
AIM
To study the role of nuclear factor-kappaB (NF-kappaB), a pro-inflammatory and anti-apoptotic factor, in IL-1-treated IEC.
METHODS
NF-kappaB activity and levels of apoptotic proteins were assessed by electrophoretic mobility shift assay and RNA-protection assay, respectively.
RESULTS
IL-1 and ceramide, which have been shown to partially mediate IL-1 effects on IEC, activated NF-kappaB levels significantly. This activation was due to a decrease in IkappaB-alpha and IkappaB-beta protein levels. Moreover, the ratio of mRNA levels of anti-apoptotic to pro-apoptotic proteins was significantly increased in IL-1-treated IEC.
CONCLUSION
NF-kappaB may play a key role in the regulation of the expression of pro-inflammatory and/or apoptotic genes in inflammatory bowel disease, making this protein an attractive target for therapeutic intervention.
摘要
背景
白细胞介素-1（IL-1）是一种炎症细胞因子，其在炎症黏膜中的水平升高，通过诱导神经酰胺生成对肠上皮细胞（IEC）产生部分作用。
目的
研究促炎和抗凋亡因子核因子-κB（NF-κB）在IL-1处理的IEC中的作用。
方法
分别通过电泳迁移率变动分析和RNA保护分析评估NF-κB活性和凋亡蛋白水平。
结果
IL-1和神经酰胺已被证明可部分介导IL-1对IEC的作用，它们显著激活了NF-κB水平。这种激活是由于IκB-α和IκB-β蛋白水平降低。此外，在IL-1处理的IEC中，抗凋亡蛋白与促凋亡蛋白的mRNA水平之比显著增加。
结论
NF-κB可能在炎症性肠病中促炎和/或凋亡基因表达的调节中起关键作用，使该蛋白成为治疗干预的有吸引力的靶点。
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