Normandie Univ, Caen, France ; UNICAEN, EA4652 MILPAT UFR de médecine, Université de Caen, Caen cedex 5, CS14032 Caen, France.
Sexmoor Laboratoires, 13 120 Saint Remy de Provence, France.
J Inflamm (Lond). 2015 Feb 23;12:17. doi: 10.1186/s12950-015-0062-7. eCollection 2015.
In inflammatory joint disease, such as osteoarthritis or arthritis, there is an increased level of pro-inflammatory cytokines, such as interleukin-1β. These cytokines stimulate the expression and release of matrix metalloproteases (MMP), leading to the degradation of cartilage extracellular matrix and subsequently mobility difficulty and suffering for patients. The aim of this study was to examine the therapeutic potential of a fatty acid copolymer in in vitro and in vivo models of cartilage inflammation.
Inflammation was mimicked in vitro by treatment of human articular chondrocytes with interleukin-1β. Effects of a co-treatment with a copolymer of fatty acids (Ara 3000 beta®) were determined by evaluating MMP production by RT-PCR and ELISA, NO release by Griess assay, and PGE2 expression by ELISA. In addition, in vivo analysis (evolution of weight and edema) were also performed after injection of Freund adjuvant in rats treated or not with the copolymer of fatty acids.
The copolymer of fatty acids clearly reduces inflammation in joint. In vitro, it impairs IL1 stimulated-MMP production and release, as well as the release of NO and PGE2 and the activation of NFκB. Furthermore, in vivo experiments using adjuvant induced-arthritis corroborates the anti-inflammatory effects of the copolymer of fatty acids, with a reduction of edemas, erythemas and ankylosis in arthritic rats.
The results support the hypothesis that a copolymer of fatty acids, such as Ara 3000 beta®, is a powerful anti-inflammatory compounds, suggesting that it has a potential for preventing cartilage degradation associated with chronic inflammatory joint disease.
在炎症性关节疾病（如骨关节炎或关节炎）中，存在促炎细胞因子（如白细胞介素-1β）水平升高。这些细胞因子刺激基质金属蛋白酶（MMP）的表达和释放，导致软骨细胞外基质降解，进而导致患者活动困难和痛苦。本研究旨在研究脂肪酸共聚物在软骨炎症的体外和体内模型中的治疗潜力。
通过用白细胞介素-1β处理人关节软骨细胞来模拟体外炎症。通过 RT-PCR 和 ELISA 评估 MMP 产生、Griess 测定法评估 NO 释放以及 ELISA 评估 PGE2 表达，来确定脂肪酸共聚物（Ara 3000 beta®）的共同处理效果。此外，还在接受或不接受脂肪酸共聚物治疗的弗氏佐剂注射大鼠中进行了体内分析（体重和水肿的演变）。
脂肪酸共聚物明显减轻关节炎症。在体外，它会损害 IL1 刺激的 MMP 产生和释放，以及 NO 和 PGE2 的释放以及 NFκB 的激活。此外，使用佐剂诱导关节炎的体内实验证实了脂肪酸共聚物的抗炎作用，关节炎大鼠的水肿、红斑和关节强直减少。
这些结果支持脂肪酸共聚物（如 Ara 3000 beta®）是一种强大的抗炎化合物的假设，表明它具有预防与慢性炎症性关节疾病相关的软骨降解的潜力。
