Abstract
Osteoarthritis (OA), defined as a long-term progressive joint disease, is characterized by cartilage impairment and erosion. In recent decades, magnolol, as a type of lignin extracted from Magnolia officinalis, has been proved to play a potent anti-inflammatory role in various diseases. The current research sought to examine the latent mechanism of magnolol and its protective role in alleviating the progress of OA in vivo as well as in vitro experimentations. In vitro, the over-production of Nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6), induced by interleukin-1 beta (IL-1β), were all inhibited notably by magnolol in a concentration-dependent manner. Moreover, magnolol could also downregulate the expression of metalloproteinase 13 (MMP13) and thrombospondin motifs 5 (ADAMTS5). All these changes ultimately led to the deterioration of the extracellular matrix (ECM) induced by IL-1β. Mechanistically, magnolol suppressed the activation of PI3K/Akt/NF-κB pathway. Furthermore, a powerful binding capacity between magnolol and PI3K was also revealed in our molecular docking research. In addition, magnolol-induced protective effects in OA development were also detected in a mouse model. In summary, this research suggested that magnolol possessed a new therapeutic potential for the development of OA.
Highlights
As a degenerative joint disease, osteoarthritis (OA) is frequently seen in the elderly population (Appleton, 2018)
The goat anti-rabbit and anti-mouse IgG-HRP were purchased from Bioworld (OH, United States), inducible nitric oxide synthase antibody was acquired from Sigma-Aldrich (St Louis, MO, United States), the primary antibody against GADPH and Lamin B1 were acquired from Abcam (CA, United Kingdom)
We used the Cell-Counting Kit-8 (CCK-8) assay to assess the viability of human chondrocytes treated with magnolol
Summary
As a degenerative joint disease, osteoarthritis (OA) is frequently seen in the elderly population (Appleton, 2018). The pathological hallmark of OA development is the articular cartilage loss, synovitis, subchondral bone recasting, and cartilage hypertrophy (Glyn-Jones et al, 2015; Flemming and Gustas-French, 2017; Scotece et al, 2018). The pathophysiology of OA is not Magnolol’s Effect in Osteoarthritis fully understood, inflammatory and inflammation-related biomarkers seem to play a critical part (Jotanovic et al, 2012). The increased secretion of IL-1β is highly detected in the OA patients’ cartilage, subchondral bone, synovial fluid, and membrane (Moos et al, 1999). New effective agents aiming to suppress IL-1β-induced inflammation or IL-1β may provide new regimens to ameliorate the progression of OA
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