Abstract

The aim of this study was to characterize the anti-inflammatory mode of action of botanical extracts from rosehip (Rosa canina), willow bark (Salix alba), and nettle leaf (Urtica dioica) in an in vitro model of primary canine articular chondrocytes. Methods. The biological effects of the botanical extracts were studied in chondrocytes treated with IL-1β for up to 72 h. Expression of collagen type II, cartilage-specific proteoglycan (CSPG), β1-integrin, SOX-9, COX-2, and MMP-9 and MMP-13 was examined by western blotting. Results. The botanical extracts suppressed IL-1β-induced NF-κB activation by inhibition of IκBα phosphorylation, IκBα degradation, p65 phosphorylation, and p65 nuclear translocation. These events correlated with downregulation of NF-κB targets including COX-2 and MMPs. The extracts also reversed the IL-1β-induced downregulation of collagen type II, CSPG, β1-integrin, and cartilage-specific transcription factor SOX-9 protein expression. In high-density cultures botanical extracts stimulated new cartilage formation even in the presence of IL-1β. Conclusions. Botanical extracts exerted anti-inflammatory and anabolic effects on chondrocytes. The observed reduction of IL-1β-induced NF-κB activation suggests that further studies are warranted to demonstrate the effectiveness of plant extracts in the treatment of OA and other conditions in which NF-κB plays pathophysiological roles.

Highlights

  • Osteoarthritis (OA) is a joint disease involving articular cartilage and the synovial membrane, subchondral bone and periarticular soft tissues [1]

  • To test IL-1β-inhibited chondrocyte proliferation an MTT assay was performed to study the effects of botanical extracts on the viability and proliferation of chondrocytes treated with or without IL-1β

  • Chondrocytes were cultured in a 96-well plate and treated with IL-1β, botanical extracts, and botanical extracts treated with IL-1β for the indicated times

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Summary

Introduction

Osteoarthritis (OA) is a joint disease involving articular cartilage and the synovial membrane, subchondral bone and periarticular soft tissues [1]. OA may occur following traumatic injury to the joint, subsequent to an infection of the joint or as a result of aging. Other sequelae include osteophyte formation and joint malalignment. These manifestations are highly variable, depending on joint location and disease severity [2]. OA is grossly characterized by aberrant synthesis of extracellular matrix, gradual hypocellularity, eventual fragmentation and degradation of cartilage, new bone formation in the periarticular region (osteophytosis), decreased, increased, subchondral bone density, and variable synovial inflammation [3]. In OA, mechanical stress initiates cartilage lesions by altering chondrocyte-matrix interaction and metabolic responses in the chondrocytes [4]

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