Abstract

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. Tabebuia avellanedae 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 (Tabebuia avellanedae ethanol extract (Ta-EE)) on OA pathogenesis induced by monoiodoacetate (MIA) and the underlying mechanisms were investigated using experiments with a rat model and in vitro 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-κB) and activator protein-1 (AP-1) signaling pathways in macrophages and chondrocytes.

Highlights

  • Osteoarthritis (OA) is a time- and age-dependent progressive degenerative joint disease characterized by the degradation of joint cartilage and the underlying bones

  • The experimental design used to explore the in vivo pharmacological effects of Ta-EE on OA pathogenesis using experimental OA rats is shown in Figure 1(a) and detailed in Sections 2.4 and 2.5

  • We investigated the in vivo pharmacological effects of Ta-EE on OA pathogenesis using an experimental OA animal model and the underlying molecular mechanisms of these effects using in vitro macrophage and chondrocyte cellular models

Read more

Summary

Introduction

Osteoarthritis (OA) is a time- and age-dependent progressive degenerative joint disease characterized by the degradation of joint cartilage and the underlying bones. OA is characterized by joint stiffness and pain caused by articular cartilage damage, the alteration of subchondral bones, formation of osteophytes, and thickening of synovial linings [1,2,3,4]. Given the current worldwide demographic trend in which the older population is growing quickly, OA patients are expected to increase in the future. Despite this large number of OA patients, no disease-modifying drugs have been developed to effectively treat OA, and the available drugs only alleviate

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call