Abstract
Osteoarthritis (OA) is a general joint illness caused by the destruction of joint cartilage, and is common in the population of old people. Its occurrence is related to inflammatory reactions and cartilage degradation. AyuFlex® is an aqueous extract of Terminalia chebula fruit, and T. chebula has been utilized extensively in several traditional oriental medications for the management of diverse diseases. Pre-clinical and clinical research has shown its antioxidant and anti-inflammatory effectiveness. Nevertheless, the mechanism underlying the anti-arthritic effects of AyuFlex® remains unclear. In the current research, we proposed the ameliorating effects of AyuFlex® with respect to the incidence of OA and described the latent signalization in interleukin (IL)-1β-treated chondrocytes and MIA-incurred OA in a rat model. In vitro, AyuFlex® decreased oxidative stress and induction of pro-inflammatory cytokines and mediators as well as matrix metalloproteinases (MMPs), while also increasing the levels of collagen synthesis-related proteins. Mechanistically, we identified that AyuFlex® disrupted nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) activation via the inhibition of NF-κB p65 and extracellular regulated protein kinase (ERK) phosphorylation. The ameliorating effects of AyuFlex® were also observed in vivo. AyuFlex® significantly inhibited the MIA-incurred increase in OA symptoms such as oxidative stress, cartilage damage, and changes in cytokines and MMPs revelation in arthrodial cartilage. Therefore, our results suggest that AyuFlex® attenuates OA progression in vivo, indicating that AyuFlex® can be suggested as an excellent therapeutic remedy for the care of OA.
Highlights
Osteoarthritis (OA) is a lingering joint illness accompanied by inflammation of the synovium and cartilage degeneration, causing physical disability in the elderly
No significant differences were observed between the six groups (Figure 6) for three weeks, and these results demonstrated that the body weight was not influenced by AyuFlex®
We report here for the first time that AyuFlex® inhibits oxidative stress, inflammation, and cartilage degradation and improves cartilage regeneration through suppressing the phosphorylation of the extracellular regulated protein kinase (ERK) and NF-κB p65 signaling pathways triggered by IL-1β in human chondrocytes
Summary
Osteoarthritis (OA) is a lingering joint illness accompanied by inflammation of the synovium and cartilage degeneration, causing physical disability in the elderly. Functional foods and medicines have been commonly utilized to care for OA, but pharmacological treatment of OA has limited effects [1,2]. Non-steroidal anti-inflammatory drugs (NSAIDs) are usually utilized for reducing inflammation and pain in OA. A long-time consumption of NSAIDs adversely affects the gastrointestinal and cardiovascular systems [3,4]. To this day, the etiology of OA is not obvious, and no effectual therapeutic treatment has been developed for OA. Safer and more effective novel agents are needed for the treatment of OA [1]
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