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      Morusin Ameliorates IL-1β-Induced Chondrocyte Inflammation and Osteoarthritis via NF-κB Signal Pathway


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          Osteoarthritis (OA) is one of the most common degenerative joint diseases in the world, characterized primarily by the progressive degradation of articular cartilage. Accumulating evidence has shown that Morusin, a flavonoid derived from the root bark of Morus alba (mulberry) plants, exerts unique protective properties in several diseases. However, its effects on OA, specifically, have not yet been characterized.


          In this study, we evaluated the anti-inflammatory effect of Morusin on mouse chondrocytes and its underlying mechanism in vitro. In addition, the protective effect of Morusin on destabilization of the medial meniscus (DMM) model was also explored in vivo.


          In vitro, IL-1β-induced activation of inflammatory factors (TNF-α, IL-6, INOS and COX2) was dramatically suppressed by Morusin. Further, Morusin treatment inhibited the expression of ADAMTS5 and metalloproteinase (MMPs), both of which regulate extracellular matrix degradation. Morusin also decreased IL-1β-induced p65 phosphorylation and IκBα degradation. In vivo, degradation of the articular cartilage following surgical DMM, which mimicked OA pathology, was abrogated following treatment with Morusin, thus demonstrating a protective effect in the DMM model.


          Herein, we demonstrate that Morusin reduces the OA inflammatory response in vitro and protects against articular cartilage degradation in vivo potentially via regulation of the NF-κB pathway. Hence, Morusin may prove to be an effective candidate for novel OA therapeutic strategies.

          Most cited references41

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          Osteoarthritis: epidemiology.

          Osteoarthritis (OA) is the most common joint disorder in the world. In Western populations it is one of the most frequent causes of pain, loss of function and disability in adults. Radiographic evidence of OA occurs in the majority of people by 65 years of age and in about 80% of those aged over 75 years. In the US it is second only to ischaemic heart disease as a cause of work disability in men over 50 years of age, and accounts for more hospitalizations than rheumatoid arthritis (RA) each year. Despite this public health impact, OA remains an enigmatic condition to the epidemiologist. In this chapter, we will review the definition and classification of OA, its prevalence, incidence, risk factors and natural history.
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            Osteoarthritis, angiogenesis and inflammation.

            Angiogenesis and inflammation are closely integrated processes in osteoarthritis (OA) and may affect disease progression and pain. Inflammation can stimulate angiogenesis, and angiogenesis can facilitate inflammation. Angiogenesis can also promote chondrocyte hypertrophy and endochondral ossification, contributing to radiographic changes in the joint. Inflammation sensitizes nerves, leading to increased pain. Innervation can also accompany vascularization of the articular cartilage, where compressive forces and hypoxia may stimulate these new nerves, causing pain even after inflammation has subsided. Inhibition of inflammation and angiogenesis may provide effective therapeutics for the treatment of OA by improving symptoms and retarding joint damage. This review aims to summarize (i) the evidence that angiogenesis and inflammation play an important role in the pathophysiology of OA and (ii) possible directions for future research into therapeutics that could effectively treat this disease.
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              Aggrecan degradation in human articular cartilage explants is mediated by both ADAMTS-4 and ADAMTS-5.

              Recent published studies have shown that cartilage from ADAMTS-5-knockout mice, but not ADAMTS-4- or ADAMTS-1-knockout mice, is significantly protected from degradation. The present study was undertaken to evaluate the respective roles of these enzymes in human cartilage breakdown, using a small interfering RNA (siRNA) approach to assess the effects of inhibition of each enzyme in normal and osteoarthritic (OA) explants. The activities of siRNA specifically targeting ADAMTS-1, -4, and -5 were assessed by transfection into primary human chondrocytes and cultured human cartilage explants. At 24 hours, a cytokine stimulus was applied to normal, but not OA, samples to initiate a catabolic response. At designated times, total RNA was isolated and gene expression was measured by quantitative real-time reverse transcription-polymerase chain reaction. Aggrecan release and aggrecanase-generated neoepitope formation were determined by dye binding analysis and Western blotting, respectively. Human chondrocytes and explants were efficiently transfected with siRNA that specifically decreased the expression of each targeted gene. Suppression of ADAMTS-4 and ADAMTS-5, individually or in combination, attenuated the degradation of aggrecan in cytokine-stimulated normal cartilage. A reduction in aggrecan degradation was also observed following siRNA-mediated knockdown of either gene in unstimulated OA cartilage. In contrast, knockdown of ADAMTS-1 failed to inhibit aggrecan loss. Despite the apparent dominant role of ADAMTS-5 in genetically modified mice, our data suggest that both ADAMTS-4 and ADAMTS-5 contribute to the structural damage that characterizes human OA.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                26 March 2020
                : 14
                : 1227-1240
                [1 ]Department of Orthopaedics, Shaoxing Hospital, Zhejiang University School of Medicine , Shaoxing, Zhejiang 312000, People’s Republic of China
                [2 ]The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University , Wenzhou, Zhejiang 325000, People’s Republic of China
                [3 ]Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University , Guangxi 530021, People’s Republic of China
                Author notes
                Correspondence: Yu Qian Department of Orthopaedics, Shaoxing Hospital, Zhejiang University School of Medicine , Shaoxing, Zhejiang312000, People’s Republic of ChinaTel +86 13905754033 Email doctor120@hotmail.com

                These authors contributed equally to this work

                © 2020 Jia et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                : 01 January 2020
                : 09 March 2020
                Page count
                Figures: 7, Tables: 1, References: 60, Pages: 14
                This study was funded by the National Natural Science Foundation of China [grant number 81572126,81871801]; the Natural Science Foundation of Zhejiang Province [grant number LY15H060005]; Natural Science Foundation of Zhejiang Province [grant number LQ16H160013]; and Zhejiang Basic Public Welfare Research Project [grand number LGF18H060010].
                Original Research

                Pharmacology & Pharmaceutical medicine
                osteoarthritis,chondrocytes,morusin,il-1β,nf-κb pathway
                Pharmacology & Pharmaceutical medicine
                osteoarthritis, chondrocytes, morusin, il-1β, nf-κb pathway


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