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      Tanshinone I Inhibits IL-1β-Induced Apoptosis, Inflammation And Extracellular Matrix Degradation In Chondrocytes CHON-001 Cells And Attenuates Murine Osteoarthritis

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          Abstract

          Background

          Osteoarthritis (OA) is a prevalent degenerative joint disease, which was characterized by inflammation and cartilage degradation. Accumulating evidence has demonstrated that Tanshinone I has an anti-inflammatory effect in various diseases. However, the efficacy of Tanshinone I as an anti-inflammatory agent in OA remains unclear. This study aimed to explore the role of Tanshinone I on OA both in vitro and in vivo.

          Methods

          CHON-001 cells were treated with IL-1β (10 ng/mL) for 72 hrs to induce OA model in vitro. Meanwhile, CHON-001 cells were pre-treated with 20 μM Tanshinone I for 24 hrs and then stimulated with IL-1β (10 ng/mL) for 72 hrs. CCK-8, immunofluorescence and flow cytometry assays were used to detect the viability, proliferation and apoptosis in CHON-001 cells, respectively. Western blotting assay was used to detect the levels of collagen II, aggrecan, MMP-13, cleaved caspase 1, Gasdermin D, SOX11 and p-NF-κB in CHON-001 cells. In addition, the mouse model of OA was built by anterior cruciate ligament transection (ACLT) in the right knee. Meanwhile, the mice were administrated with 10 or 30 mg/kg Tanshinone I for 8 weeks. Safranin-O/Fast Green staining was used to assess cartilage destruction in a mouse model of OA.

          Results

          In this study, IL-1β significantly induced apoptosis, extracellular matrix degradation and inflammatory response in CHON-001 cells. Tanshinone I significantly inhibited IL-1β-induced apoptosis in CHON-001 cells. In addition, the IL-1β-induced collagen II, aggrecan degradation, SOX11 downregulation, and MMP-13 and p-NF-κB upregulation in CHON-001 cells were notably reversed by Tanshinone I treatment. Moreover, Tanshinone I alleviated cartilage destruction and synovitis and reduced OARSI scores and subchondral bone thickness in a mouse model of OA.

          Conclusion

          Our findings showed that Tanshinone I could alleviate the progression of OA in vitro and in vivo. These results demonstrated that Tanshinone I might be regarded as a promising therapeutic agent for the treatment of OA.

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          Most cited references 32

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          Osteoarthritis cartilage histopathology: grading and staging.

          Current osteoarthritis (OA) histopathology assessment methods have difficulties in their utility for early disease, as well as their reproducibility and validity. Our objective was to devise a more useful method to assess OA histopathology that would have wide application for clinical and experimental OA assessment and would become recognized as the standard method. An OARSI Working Group deliberated on principles, standards and features for an OA cartilage pathology assessment system. Using current knowledge of the pathophysiology of OA morphologic features, a proposed system was presented at OARSI 2000. Subsequently, this was widely circulated for comments amongst experts in OA pathology. An OA cartilage pathology assessment system based on six grades, which reflect depth of the lesion and four stages reflecting extent of OA over the joint surface was developed. The OARSI cartilage OA histopathology grading system appears consistent and simple to apply. Further studies are required to confirm the system's utility.
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            The Role of Inflammatory and Anti-Inflammatory Cytokines in the Pathogenesis of Osteoarthritis

            Osteoarthritis (OA) is the most common chronic disease of human joints. The basis of pathologic changes involves all the tissues forming the joint; already, at an early stage, it has the nature of inflammation with varying degrees of severity. An analysis of the complex relationships indicates that the processes taking place inside the joint are not merely a set that (seemingly) only includes catabolic effects. Apart from them, anti-inflammatory anabolic processes also occur continually. These phenomena are driven by various mediators, of which the key role is attributed to the interactions within the cytokine network. The most important group controlling the disease seems to be inflammatory cytokines, including IL-1 β , TNF α , IL-6, IL-15, IL-17, and IL-18. The second group with antagonistic effect is formed by cytokines known as anti-inflammatory cytokines such as IL-4, IL-10, and IL-13. The role of inflammatory and anti-inflammatory cytokines in the pathogenesis of OA with respect to inter- and intracellular signaling pathways is still under investigation. This paper summarizes the current state of knowledge. The cytokine network in OA is put in the context of cells involved in this degenerative joint disease. The possibilities for further implementation of new therapeutic strategies in OA are also pointed.
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              Integrative MicroRNA and Proteomic Approaches Identify Novel Osteoarthritis Genes and Their Collaborative Metabolic and Inflammatory Networks

              Background Osteoarthritis is a multifactorial disease characterized by destruction of the articular cartilage due to genetic, mechanical and environmental components affecting more than 100 million individuals all over the world. Despite the high prevalence of the disease, the absence of large-scale molecular studies limits our ability to understand the molecular pathobiology of osteoathritis and identify targets for drug development. Methodology/Principal Findings In this study we integrated genetic, bioinformatic and proteomic approaches in order to identify new genes and their collaborative networks involved in osteoarthritis pathogenesis. MicroRNA profiling of patient-derived osteoarthritic cartilage in comparison to normal cartilage, revealed a 16 microRNA osteoarthritis gene signature. Using reverse-phase protein arrays in the same tissues we detected 76 differentially expressed proteins between osteoarthritic and normal chondrocytes. Proteins such as SOX11, FGF23, KLF6, WWOX and GDF15 not implicated previously in the genesis of osteoarthritis were identified. Integration of microRNA and proteomic data with microRNA gene-target prediction algorithms, generated a potential “interactome” network consisting of 11 microRNAs and 58 proteins linked by 414 potential functional associations. Comparison of the molecular and clinical data, revealed specific microRNAs (miR-22, miR-103) and proteins (PPARA, BMP7, IL1B) to be highly correlated with Body Mass Index (BMI). Experimental validation revealed that miR-22 regulated PPARA and BMP7 expression and its inhibition blocked inflammatory and catabolic changes in osteoarthritic chondrocytes. Conclusions/Significance Our findings indicate that obesity and inflammation are related to osteoarthritis, a metabolic disease affected by microRNA deregulation. Gene network approaches provide new insights for elucidating the complexity of diseases such as osteoarthritis. The integration of microRNA, proteomic and clinical data provides a detailed picture of how a network state is correlated with disease and furthermore leads to the development of new treatments. This strategy will help to improve the understanding of the pathogenesis of multifactorial diseases such as osteoarthritis and provide possible novel therapeutic targets.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                DDDT
                dddt
                Drug Design, Development and Therapy
                Dove
                1177-8881
                15 October 2019
                2019
                : 13
                : 3559-3568
                Affiliations
                [1 ]Department of Orthopaedic Surgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology , Wuhan 430010, People’s Republic of China
                [2 ]Department of Orthopaedic Surgery, The Second Affiliated Hospital of Nantong University , Nantong, Jiangsu 226001, People’s Republic of China
                Author notes
                Correspondence: Wei Liu Department of Orthopaedic Surgery, The Second Affiliated Hospital of Nantong University , Nantong, Jiangsu226001, People’s Republic of China Email weiliu_111@126.com
                Article
                216596
                10.2147/DDDT.S216596
                6800556
                © 2019 Wang 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: 45, Pages: 10
                Categories
                Original Research

                Pharmacology & Pharmaceutical medicine

                chondrocytes, osteoarthritis, tanshinone i, il-1β

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