Homaidan Fadia R, Chakroun Iman, El-Sabban Marwan E
Department of Physiology, American University of Beirut, Faculty of Medicine, Beirut, Lebanon.
Mediators Inflamm. 2003 Oct;12(5):277-83. doi: 10.1080/09629350310001619681.
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.
To study the role of nuclear factor-kappaB (NF-kappaB), a pro-inflammatory and anti-apoptotic factor, in IL-1-treated IEC.
NF-kappaB activity and levels of apoptotic proteins were assessed by electrophoretic mobility shift assay and RNA-protection assay, respectively.
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.
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.
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。
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。
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。
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。
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。
