Abstract

Kaempferia parviflora Wall. ex Baker (KP) has been reported to attenuate cartilage destruction in rat model of osteoarthritis. Previously, we demonstrated that KP rhizome extract and its active components effectively suppressed mechanisms associated with RA in SW982 cells. Here, we further evaluated the anti-arthritis potential of KP extract by using multi-level models, including a complete Freund’s adjuvant-induced arthritis and a cartilage explant culture model, and to investigate the effects of KP extract and its major components on related gene expressions and underlying mechanisms within cells. In arthritis rats, the KP extract reduced arthritis indexes, with no significant changes in biological parameters. In the cartilage explant model, the KP extract exerted chondroprotective potential by suppressing sulfated glycosaminoglycans release while preserving high accumulation of proteoglycans. In human chondrocyte cell line, a mixture of the major components equal to their amounts in KP extract showed strong suppression the expression of genes-associated inflammatory joint disease similar to that of the extract. Additionally, KP extract significantly suppressed NF-κB and MAPK signaling pathways. The suppressing expression of necroptosis genes and promoted anti-apoptosis were also found. Collectively, these results provided supportive evidence of the anti-arthritis properties of KP extract, which are associated with its three major components.

Highlights

  • Arthritis is defined as joint inflammation that is generally accompanied by cartilage and joint damage [1]

  • We further investigated the molecular actions of the KP extract and its major components in signal transductions of the NF-κB and mitogen-activated protein kinase (MAPK) pathways, which are involved in the pathogenesis of arthritis

  • Regarding the signaling pathways involved in the anti-arthritis effects, the KP extract showed strong selective suppression of the phosphorylation of some proteins, which involves the NF-κB and MAPK pathways

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Summary

Introduction

Arthritis is defined as joint inflammation that is generally accompanied by cartilage and joint damage [1]. Two of the most common forms of arthritis are osteoarthritis (OA) and rheumatoid arthritis (RA) [1] They share some similar features, including joint pain, inflammation, and cartilage breakdown [2]. These arthritis forms can be differentiated by their clinical appearance and molecular mechanism of pathogenesis. RA involves the systemic autoimmune disorders targeting the synovial tissue lining of the joint capsule that lead to chronic highgrade systemic inflammation and progressive damage to cartilage and bone, which results in permanent joint disability [1]

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