Department of Genetic Engineering, Sungkyunkwan University, Suwon 16419, Republic of Korea.
Department of Pharmaceutical Engineering, Cheongju University, Cheongju 28503, Republic of Korea.
Mediators Inflamm. 2017;2017:3619879. doi: 10.1155/2017/3619879. Epub 2017 Nov 26.
Although osteoarthritis (OA), a degenerative joint disease characterized by the degradation of joint articular cartilage and subchondral bones, is generally regarded as a degenerative rather than inflammatory disease, recent studies have indicated the involvement of inflammation in OA pathogenesis. has long been used to treat various diseases; however, its role in inflammatory response and the underlying molecular mechanisms remain poorly understood. In this study, the pharmacological effects of Tabetri ( ethanol extract (Ta-EE)) on OA pathogenesis induced by monoiodoacetate (MIA) and the underlying mechanisms were investigated using experiments with a rat model and cellular models. In the animal model, Ta-EE significantly ameliorated OA symptoms and reduced the serum levels of inflammatory mediators and proinflammatory cytokines without any toxicity. The anti-inflammatory activity of Ta-EE was further confirmed in a macrophage-like cell line (RAW264.7). Ta-EE dramatically suppressed the production and mRNA expressions of inflammatory mediators and proinflammatory cytokines in lipopolysaccharide-stimulated RAW264.7 cells without any cytotoxicity. Finally, the chondroprotective effect of Ta-EE was examined in a chondrosarcoma cell line (SW1353). Ta-EE markedly suppressed the mRNA expression of matrix metalloproteinase genes. The anti-inflammatory and chondroprotective activities of Ta-EE were attributed to the targeting of the nuclear factor-kappa B (NF-B) and activator protein-1 (AP-1) signaling pathways in macrophages and chondrocytes.
虽然骨关节炎(OA)是一种以关节软骨和软骨下骨降解为特征的退行性关节疾病,通常被认为是一种退行性而非炎症性疾病,但最近的研究表明炎症参与了 OA 的发病机制。 已经被用于治疗各种疾病;然而,其在炎症反应中的作用及其潜在的分子机制仍知之甚少。在这项研究中,使用大鼠模型和细胞模型研究了 Tabetri(乙醇提取物(Ta-EE))对单碘乙酸(MIA)诱导的 OA 发病机制的药理作用及其潜在机制。在动物模型中,Ta-EE 显著改善了 OA 症状,降低了炎症介质和促炎细胞因子的血清水平,没有任何毒性。Ta-EE 的抗炎活性在巨噬细胞样细胞系(RAW264.7)中得到了进一步证实。Ta-EE 可显著抑制脂多糖刺激的 RAW264.7 细胞中炎症介质和促炎细胞因子的产生和 mRNA 表达,而没有任何细胞毒性。最后,在软骨肉瘤细胞系(SW1353)中检查了 Ta-EE 的软骨保护作用。Ta-EE 显著抑制基质金属蛋白酶基因的 mRNA 表达。Ta-EE 的抗炎和软骨保护作用归因于其在巨噬细胞和软骨细胞中靶向核因子-kappa B(NF-B)和激活蛋白-1(AP-1)信号通路。