Bromelain Extract Exerts Antiarthritic Effects via Chondroprotection and the Suppression of TNF-α-Induced NF-κB and MAPK Signaling.

Peraphan Pothacharoen,Rujirek Chaiwongsa,Pilanee Vaithanomsat,Phornpimon Janchai,Orapin Insuan,Thanchanok Wongwichai,Theerawut Chanmee

doi:10.3390/plants10112273

Peraphan Pothacharoen, Rujirek Chaiwongsa + Show 5 more

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https://doi.org/10.3390/plants10112273

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Abstract

Bromelain, a mixture of proteases in pineapple rhizome, has beneficial biological properties. Following absorption, the compound remains biologically active in mammalian blood and tissues. Bromelain has multiple clinical and therapeutic applications because of its anti-arthritic activities. Anti-inflammation is one of the putative therapeutic effects of bromelain on osteoarthritis (OA) and rheumatoid arthritis (RA), but the molecular mechanisms in cartilage and synovial fibroblast has not been reported. Thus, in this study, interleukin (IL)-1β/oncostatin M-induced porcine cartilage and TNF-α–induced synovial fibroblast were used as the inflamed OA and RA models, respectively. The results demonstrated the chondroprotective effects of bromelain on cartilage degradation and the downregulation of inflammatory cytokine (tumor necrosis factor (TNF)-α, IL-1β, IL-6, IL-8) expression in TNF-α–induced synovial fibroblasts by suppressing NF-κB and MAPK signaling. The evidence from this study supported and explained the anti-inflammatory and analgesic effects of bromelain on arthritis in animal models and clinical studies.

Highlights

Rhizome bromelain contains higher levels of proteases than bromelain derived from the fruit
The HPLC profile revealed that the bromelain extract used in this study was identical to stem bromelain, and the peak of bromelain extract appeared at a retention time of 0.9 min
The bromelain extract examined in this study was previously characterized for protease activity, and its molecular weight was calculated as 25–27 kDa [10]

Summary

Introduction

Are the most common prevalent disorders of the articular joints, and they cause disability and increase medical costs in elderly people. Proinflammatory cytokine-induced inflammation is the hallmark of both OA and RA. OA is a whole-joint disease resulting in alteration of the structure of hyaline cartilage, subchondral bone, ligaments, capsules, synovial tissues, and periarticular muscles. Interleukin (IL)-1β participates in the pathogenesis of OA by upregulating matrix-degrading degraded enzymes (matrix metalloproteinases (MMPs), ADAMTS) and suppressing matrix molecules synthesis [1,2]. RA is typified by chronic inflammation of the lining of the joints with synovial inflammation and hyperplasia, hyaline cartilage degradation, bone destruction, and systemic features, including cardiovascular, pulmonary, psychological, and skeletal disorders. Tumor necrosis factor (TNF)-α is a proinflammatory cytokine plays a pivotal role in regulating the inflammatory response in RA [3]

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