Abstract
BackgroundIn 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.MethodsInflammation 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.ResultsThe 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.ConclusionsThe 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.
Highlights
In inflammatory joint disease, such as osteoarthritis or arthritis, there is an increased level of pro-inflammatory cytokines, such as interleukin-1β
IL-1β has been detected in the synovial fluid of OA patients [1] and plays a major role in joint diseases, causing overproduction of prostaglandin E2 (PGE2), reactive oxygen species (ROS), nitric oxide (NO), and matrix metalloproteases (MMP), which all contribute to the degradative process of cartilage
We evaluated its effects on IL-1-induced MMP production and other markers of inflammation in articular chondrocyte culture
Summary
In inflammatory joint disease, such as osteoarthritis or arthritis, there is an increased level of pro-inflammatory cytokines, such as interleukin-1β. IL-1β reduces levels of inhibitors of MMPs (tissue inhibitors of MMPs, TIMP) in arthritic joints and decreases biosynthesis of type II collagen and aggrecan, limiting the repair potential of cartilage These effects have been confirmed by in vivo studies showing that intraarticular administration of IL-1β into animal. Baugé et al Journal of Inflammation (2015) 12:17 joints causes proteoglycan loss from the cartilage, whereas injection of IL-1 receptor antagonist (IL-1ra) protects cartilage in arthritic joints Regarding these data, numerous in vitro studies have evaluated the interest of anti-arthritic molecules using their ability to counteract IL-1 effects in models of inflammatory joint diseases. Even if IL-1β is a crucial factor in cartilage degradation mechanisms, other proinflammatory cytokines, especially TNF-α and IL6, play major roles and can strongly stimulate inflammation in arthritis
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