University of Liège, Institute of Pathology, Sart-Tilman, Liège, Belgium.
Osteoarthritis Cartilage. 2010 Feb;18(2):141-9. doi: 10.1016/j.joca.2009.10.002. Epub 2009 Oct 8.
Curcumin (diferuloylmethane) is the principal biochemical component of the spice turmeric and has been shown to possess potent anti-catabolic, anti-inflammatory and antioxidant, properties. This article aims to provide a summary of the actions of curcumin on articular chondrocytes from the available literature with the use of a text-mining tool. We highlight both the potential benefits and drawbacks of using this chemopreventive agent for treating osteoarthritis (OA). We also explore the recent literature on the molecular mechanisms of curcumin mediated alterations in gene expression mediated via activator protein 1 (AP-1)/nuclear factor-kappa B (NF-kappaB) signalling in chondrocytes, osteoblasts and synovial fibroblasts.
A computer-aided search of the PubMed/Medline database aided by a text-mining tool to interrogate the ResNet Mammalian database 6.0.
Recent work has shown that curcumin protects human chondrocytes from the catabolic actions of interleukin-1 beta (IL-1beta) including matrix metalloproteinase (MMP)-3 up-regulation, inhibition of collagen type II and down-regulation of beta1-integrin expression. Curcumin blocks IL-1beta-induced proteoglycan degradation, AP-1/NF-kappaB signalling, chondrocyte apoptosis and activation of caspase-3.
The available data from published in vitro and in vivo studies suggest that curcumin may be a beneficial complementary treatment for OA in humans and companion animals. Nevertheless, before initiating extensive clinical trials, more basic research is required to improve its solubility, absorption and bioavailability and gain additional information about its safety and efficacy in different species. Once these obstacles have been overcome, curcumin and structurally related biochemicals may become safer and more suitable nutraceutical alternatives to the non-steroidal anti-inflammatory drugs that are currently used for the treatment of OA.
姜黄素（二芳基甲烷）是香料姜黄的主要生化成分，已被证明具有强大的抗分解代谢、抗炎和抗氧化特性。本文旨在通过文本挖掘工具，从现有文献中总结姜黄素对关节软骨细胞的作用。我们强调了使用这种化学预防剂治疗骨关节炎（OA）的潜在益处和缺点。我们还探讨了姜黄素介导的基因表达改变的分子机制的最新文献，这些改变是通过软骨细胞、成骨细胞和滑膜成纤维细胞中的激活蛋白 1（AP-1）/核因子-κB（NF-κB）信号传导介导的。
通过计算机辅助搜索 PubMed/Medline 数据库，并使用文本挖掘工具查询 ResNet 哺乳动物数据库 6.0。
最近的研究表明，姜黄素可以保护人软骨细胞免受白细胞介素-1β（IL-1β）的分解代谢作用，包括基质金属蛋白酶（MMP）-3 的上调、胶原 II 的抑制和β1-整合素表达的下调。姜黄素阻断 IL-1β诱导的蛋白聚糖降解、AP-1/NF-κB 信号传导、软骨细胞凋亡和 caspase-3 的激活。
已发表的体外和体内研究数据表明，姜黄素可能是人类和伴侣动物 OA 的有益补充治疗方法。然而，在开始广泛的临床试验之前，需要进行更多的基础研究，以提高其溶解度、吸收和生物利用度，并获得有关其在不同物种中的安全性和疗效的更多信息。一旦克服了这些障碍，姜黄素和结构上相关的生化物质可能成为更安全、更适合的营养替代品，替代目前用于治疗 OA 的非甾体抗炎药。
