Glucosamine modulates IL-1-induced activation of rat chondrocytes at a receptor level, and by inhibiting the NF-κB pathway
Glucosamine modulates IL-1-induced activation of rat chondrocytes at a receptor level, and by inhibiting the NF-κB pathway
复制标题
DOI：
10.1016/s0014-5793(01)03255-0
复制
发表时间：
2002-01-16
期刊：
影响因子：
3.5
通讯作者：
Bordji, K
中科院分区：
文献类型：
--
作者：
Gouze, JN;Bianchi, A;Bordji, K
我们最近报道，氨基葡萄糖逆转了由白细胞介素1β(IL-1β)[关节炎大黄]引起的蛋白多糖合成和UDP-葡萄糖醛酸基转移酶I基因表达的下降。44(2001)351-360]。在目前的工作中，我们证明了氨基葡萄糖不会在软骨细胞受到活性氧(ROS)刺激时发挥同样的作用。为了更好地了解其作用机制，我们确定了氨基葡萄糖是否可以阻止IL-1β与其细胞受体的结合，或者是否可以在受体后水平干扰其信号通路。在经IL-1β或ROS处理的大鼠软骨细胞中添加氨基葡萄糖可降低核因子kappaB的活性，但不会降低激活蛋白-1的活性。经IL-1β处理后，氨基葡萄糖增加了编码II型IL-1β受体的mRNA的表达。这些结果强调了IL-1β信号通路的两个调节蛋白的潜在作用，这可能解释了氨基葡萄糖在骨关节炎中的有益作用。(C)2002年欧洲生化学会联合会。爱思唯尔科学公司出版。版权所有。
We recently reported that glucosamine reversed the decrease in proteoglycan synthesis and in UDP-glucuronosyl- transferase I mRNA expression induced by interleukin-1beta (IL-1beta) [Arthritis Rheum. 44 (2001) 351-360]. In the present work, we show that glucosamine does not exert the same effects when chondrocytes; were stimulated with reactive oxygen species (ROS). In order to better understand its mechanism of action, we determined if glucosamine could prevent the binding of IL-1beta to its cellular receptors or could interfere with its signaling pathway at a post-receptor level. Addition of glucosamine to rat chondrocytes treated with IL-1beta or with ROS decreased the activation of the nuclear factor kappaB, but not the activator protein-1. After treatment with IL-1beta, glucosamine increased the expression of mRNA encoding the type II IL-1beta receptor. These results emphasize the potential role of two regulating proteins of the IL-1beta signaling pathway that could account for the beneficial effect of glucosamine in osteoarthritis. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.