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      Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats

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          Osteoarthritis (OA) is the most common disease, which seriously affects the daily life of the elderly. Currently, no traditional or drug therapy has been shown to explicitly block the progression of OA. Salidroside (Sal) is a bioactive component of Rhodiola rosea, which has many beneficial effects on human health. However, the role and mechanism of Sal in OA have not been reported.


          We established an anterior cruciate ligament transection (ACLT)-induced OA Rat model. The rats were divided into five groups (n = 10): Control group; ACLT group; ACLT + Sal (12.5 mg/kg) group; ACLT + Sal (25 mg/kg) group; ACLT + Sal (50 mg/kg) group.


          The study showed that Sal could significantly promote the proliferation of chondrocytes in OA rats induced by ACLT and restore the histological alteration of cartilage. Besides, Sal upregulated the levels of Collagen II and Aggrecan, and downregulated the level of MMP-13. Furthermore, Sal could reduce the number of CD4+IL-17 + cells and decrease the levels of IL-17, IKBα and p65, while elevating the number of CD4+IL-10 + cells and the level of IL-10. The decrease of IL-17 further inhibited the dissociation of IKBα to p65, thus reducing the release of TNF-α and VCAM-1. Taken together, Sal alleviates cartilage degeneration through promoting chondrocytes proliferation, inhibiting collagen fibrosis, and regulating inflammation and immune responses via NF-κB pathway in ACLT-induced OA Rats.


          Collectively, our study investigates the role and mechanism of Sal in OA, which lays a foundation for the application of Sal in OA.

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          Most cited references 39

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          Effect of Intra-articular Triamcinolone vs Saline on Knee Cartilage Volume and Pain in Patients With Knee Osteoarthritis: A Randomized Clinical Trial.

           Timothy McAlindon (corresponding) ,  Michael LaValley,  William F Harvey (2017)
          Synovitis is common and is associated with progression of structural characteristics of knee osteoarthritis. Intra-articular corticosteroids could reduce cartilage damage associated with synovitis but might have adverse effects on cartilage and periarticular bone.
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            The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand.

            Clinical criteria for the classification of symptomatic idiopathic (primary) osteoarthritis (OA) of the hands were developed from data collected in a multicenter study. Patients with OA were compared with a group of patients who had hand symptoms from other causes, such as rheumatoid arthritis and the spondylarthropathies. Variables from the medical history, physical examination, laboratory tests, and radiographs were analyzed. All patients had pain, aching, or stiffness in the hands. Patients were classified as having clinical OA if on examination there was hard tissue enlargement involving at least 2 of 10 selected joints, swelling of fewer than 3 metacarpophalangeal joints, and hard tissue enlargement of at least 2 distal interphalangeal (DIP) joints. If the patient had fewer than 2 enlarged DIP joints, then deformity of at least 1 of the 10 selected joints was necessary in order to classify the symptoms as being due to OA. The 10 selected joints were the second and third DIP, the second and third proximal interphalangeal, and the trapeziometacarpal (base of the thumb) joints of both hands. Criteria derived using the "classification tree" method were 92% sensitive and 98% specific. The "traditional format" classification method required that at least 3 of these 4 criteria be present to classify a patient as having OA of the hand. The latter sensitivity was 94% and the specificity was 87%. Radiography was of less value than clinical examination in the classification of symptomatic OA of the hands.
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              Roles of inflammatory and anabolic cytokines in cartilage metabolism: signals and multiple effectors converge upon MMP-13 regulation in osteoarthritis.

              Human cartilage is a complex tissue of matrix proteins that vary in amount and orientation from superficial to deep layers and from loaded to unloaded zones. A major challenge to efforts to repair cartilage by stem cell-based and other tissue engineering strategies is the inability of the resident chondrocytes to lay down new matrix with the same structural and resilient properties that it had upon its original formation. This is particularly true of the collagen network, which is susceptible to cleavage once proteoglycans are depleted. Thus, a thorough understanding of the similarities and particularly the marked differences in mechanisms of cartilage remodeling during development, osteoarthritis, and aging may lead to more effective strategies for preventing cartilage damage and promoting repair. To identify and characterize effectors or regulators of cartilage remodeling in these processes, we are using culture models of primary human and mouse chondrocytes and cell lines and mouse genetic models to manipulate gene expression programs leading to matrix remodeling and subsequent chondrocyte hypertrophic differentiation, pivotal processes which both go astray in OA disease. Matrix metalloproteinases (MMP)-13, the major type II collagen-degrading collagenase, is regulated by stress-, inflammation-, and differentiation-induced signals that not only contribute to irreversible joint damage (progression) in OA, but importantly, also to the initiation/onset phase, wherein chondrocytes in articular cartilage leave their natural growth- and differentiation-arrested state. Our work points to common mediators of these processes in human OA cartilage and in early through late stages of OA in surgical and genetic mouse models.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                14 April 2020
                : 14
                : 1445-1454
                [1 ]Department of Orthopaedics, Tinglin Hospital , Shanghai 201505, People’s Republic of China
                [2 ]Department of Orthopaedics, Hospital of Traditional Chinese Medicine, E’dong Healthcare Group , Huangshi 435000, People’s Republic of China
                [3 ]Department of Rehabilitation, Hanchuan People’s Hospital , Hanchuan, 431600, People’s Republic of China
                Author notes
                Correspondence: Ping Li Department of Rehabilitation, Hanchuan People’s Hospital , NO.1 Renmin Avenue, Hanchuan City, Hubei Province, People’s Republic of ChinaTel +86-18371202625 Email kezzajps2jf@sina.com

                These authors contributed equally to this work

                © 2020 Gao 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).

                Page count
                Figures: 5, References: 44, Pages: 10
                Original Research


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