lignans and Osteoarthritis

lignans has been researched along with Osteoarthritis* in 10 studies

Other Studies

10 other study(ies) available for lignans and Osteoarthritis

ArticleYear
Syringaresinol attenuates osteoarthritis via regulating the NF-κB pathway.
    International immunopharmacology, 2023, Volume: 118

    Osteoarthritis (OA) is a now regarded as a worldwide whole joint disease with synovial inflammation, cartilage degeneration, and subchondral sclerosis. Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used drugs for OA treatment which only relieve the symptoms and restrain the progression of OA. However, various severe adverse effects often occur in patients with long-term NSAIDs use, which heavily burdens the healthcare system and impacts the quality of life. Therefore, it is much imperative to identify alternative drugs with increased efficacy. Syringaresinol (Syr), a naturally occurring phytochemical which belonging to the lignan group of polyphenols, shows anti-tumor and anti-oxidant activities, which to benefit human health. Studies has shown Syr can regulate the inflammatory response by modulating the secretion and expression level of cytokines IL-6, IL-8, and tumor necrosis factor (TNF)-α. it also shows the inhibitory effect on NF-κB pathway in mouse cells. In the present study, we aimed to demonstrate the anti-inflammatory effects of Syr in OA. In vitro Syr treatment in IL-1β-activated mouse chondrocytes significantly restrained the expression of NO, PGE2, IL-6, TNF-α, INOS, COX-2 and MMP-13. Moreover, it considerably ameliorated the degradation of aggrecan and collagen II. Furthermore, the phosphorylation of the NF-kB signaling pathway was significantly suppressed by Syr. Moreover, in vivo, the cartilage degeneration was attenuated and the increased Osteoarthritis Research Society International (OARSI) scores were reversed in the DMM + Syr group, comprared to those in the DMM group. In sum, our study demonstrated that Syr can attenuate the inflammation in vitro and further verified its effect on OA in vivo. Thus, Syr might be a potent therapeautic alternative for OA treatment.

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cells, Cultured; Chondrocytes; Humans; Inflammation; Interleukin-1beta; Interleukin-6; Lignans; Mice; NF-kappa B; Osteoarthritis; Quality of Life

2023
Fargesin ameliorates osteoarthritis via macrophage reprogramming by downregulating MAPK and NF-κB pathways.
    Arthritis research & therapy, 2021, 05-14, Volume: 23, Issue:1

    To investigate the role and regulatory mechanisms of fargesin, one of the main components of Magnolia fargesii, in macrophage reprogramming and crosstalk across cartilage and synovium during osteoarthritis (OA) development.. Ten-week-old male C57BL/6 mice were randomized and assigned to vehicle, collagenase-induced OA (CIOA), or CIOA with intra-articular fargesin treatment groups. Articular cartilage degeneration was evaluated using the Osteoarthritis Research Society International (OARSI) score. Immunostaining and western blot analyses were conducted to detect relative protein. Raw264.7 cells were treated with LPS or IL-4 to investigate the role of polarized macrophages. ADTC5 cells were treated with IL-1β and conditioned medium was collected to investigate the crosstalk between chondrocytes and macrophages.. Fargesin attenuated articular cartilage degeneration and synovitis, resulting in substantially lower Osteoarthritis Research Society International (OARSI) and synovitis scores. In particular, significantly increased M2 polarization and decreased M1 polarization in synovial macrophages were found in fargesin-treated CIOA mice compared to controls. This was accompanied by downregulation of IL-6 and IL-1β and upregulation of IL-10 in serum. Conditioned medium (CM) from M1 macrophages treated with fargesin reduced the expression of matrix metalloproteinase-13, RUNX2, and type X collagen and increased Col2a1 and SOX9 in OA chondrocytes, but fargesin alone did not affect chondrocyte catabolic processes. Moreover, fargesin exerted protective effects by suppressing p38/ERK MAPK and p65/NF-κB signaling.. This study showed that fargesin switched the polarized phenotypes of macrophages from M1 to M2 subtypes and prevented cartilage degeneration partially by downregulating p38/ERK MAPK and p65/NF-κB signaling. Targeting macrophage reprogramming or blocking the crosstalk between macrophages and chondrocytes in early OA may be an effective preventive strategy.

    Topics: Animals; Benzodioxoles; Cartilage, Articular; Chondrocytes; Interleukin-1beta; Lignans; Macrophages; Male; Mice; Mice, Inbred C57BL; NF-kappa B; Osteoarthritis

2021
A network pharmacology strategy to investigate the anti-osteoarthritis mechanism of main lignans components of Schisandrae Fructus.
    International immunopharmacology, 2021, Volume: 98

    Osteoarthritis (OA) is a chronic age-related progressive joint disorder. Degradation of the cartilage extracellular matrix (ECM) is considered a hallmark of OA and may be a target for new therapeutic methods. Schisandrae Fructus (SF) has been shown to be effective in treating OA. The major active components of SF are lignans. However, the targets of SF and the pharmacological mechanisms underlying the effects of SF lignans in the treatment of OA have not been elucidated. Therefore, based on network pharmacology, this research predicted the treatment targets of six lignans in SF, constructed a protein-protein interaction network and identified 15 hub genes in the OA-target protein-protein interaction network. Through Gene Ontology function and pathway analyses, the gene functions of lignans in the treatment of OA were determined. Finally, the anti-OA effects of lignans and underlying mechanisms identified in the network pharmacology analysis were verified by molecular docking, real-time PCR and western blotting in vitro. The biological processes of the genes and proteins targeted by lignans in the treatment of OA included the immune response, inflammatory response, cell signal transduction and phospholipid metabolism. Moreover, 20 metabolic pathways were enriched. Network pharmacology, molecular docking and in vitro and in vivo experimental results revealed that SF, schisanhenol and gamma-schisandrin inhibited EGFR and MAPK14 gene expression by inhibiting SRC gene expression and activity and then decreased MMP 13 and collagen II protein and gene expression. This research provides a basis for further study of the anti-OA effects and mechanisms of SF, schisanhenol and gamma-schisandrin.

    Topics: Animals; Arthritis, Experimental; Fruit; Humans; Lignans; Male; Mice; Molecular Docking Simulation; Network Pharmacology; Osteoarthritis; Papain; Plant Extracts; Protein Interaction Maps; Schisandra

2021
Arctigenin prevents the progression of osteoarthritis by targeting PI3K/Akt/NF-κB axis: In vitro and in vivo studies.
    Journal of cellular and molecular medicine, 2020, Volume: 24, Issue:7

    Osteoarthritis (OA), which is principally featured by progressive joint metabolic imbalance and subsequent degeneration of articular cartilage, is a common chronic joint disease. Arctigenin (ATG), a dietary phyto-oestrogen, has been described to have potent anti-inflammatory effects. Nevertheless, its protective effects on OA have not been clearly established. The target of our following study is to evaluate the protective effects of ATG on IL-1β-induced human OA chondrocytes and mouse OA model. Our results revealed that the ATG pre-treatment effectively decreases the level of pro-inflammatory mediators, such as prostaglandin E2 (PGE2), nitrous oxide (NO), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), IL-6 and tumour necrosis factor alpha (TNF-α) in IL-1β-induced human chondrocytes. In addition, ATG protects against the degradation of extracellular matrix (ECM) under the stimulation of IL-1β and the possible mechanism might be connected with the inactivation of phosphatidylinositol-3-kinase (PI3K)/Akt/nuclear factor-kappa B (NF-κB) axis. Furthermore, a powerful binding capacity between ATG and PI3K was also uncovered in our molecular docking research. Meanwhile, ATG may act as a protector on the mouse OA model. Collectively, all these findings suggest that ATG could be utilized as a promising therapeutic agent for the treatment of OA.

    Topics: Animals; Cartilage, Articular; Chondrocytes; Dinoprostone; Disease Models, Animal; Disease Progression; Furans; Humans; Inflammation; Interleukin-1beta; Interleukin-6; Lignans; Mice; Molecular Docking Simulation; NF-kappa B; Nitric Oxide Synthase Type II; Nitrous Oxide; Osteoarthritis; Phosphatidylinositol 3-Kinases; Primary Cell Culture; Proto-Oncogene Proteins c-akt; Signal Transduction

2020
3D-Printed Extracellular Matrix/Polyethylene Glycol Diacrylate Hydrogel Incorporating the Anti-inflammatory Phytomolecule Honokiol for Regeneration of Osteochondral Defects.
    The American journal of sports medicine, 2020, Volume: 48, Issue:11

    Osteoarthritis is the leading cause of disability worldwide; cartilage degeneration and defects are the central features. Significant progress in tissue engineering holds promise to regenerate damaged cartilage tissue. However, a formidable challenge is to develop a 3-dimensional (3D) tissue construct that can regulate local immune environment to facilitate the intrinsic osteochondral regeneration.. To evaluate efficacy of a 3D-printed decellularized cartilage extracellular matrix (ECM) and polyethylene glycol diacrylate (PEGDA) integrated novel scaffold (PEGDA/ECM) together with the natural compound honokiol (Hon) for regenerating osteochondral defect.. Controlled laboratory study.. We used a stereolithography-based 3D printer for PEGDA/ECM bioprinting. A total of 36 Sprague-Dawley rats with cylindrical osteochondral defect in the trochlear groove of the femur were randomly assigned into 3 different treatments: no scaffold implantation (Defect group), 3D printed PEGDA/ECM scaffold alone (PEGDA/ECM group), or Hon suspended in a 3D-printed PEGDA/ECM scaffold (PEGDA/ECM/Hon group). 12 rats that underwent only medial parapatellar incision surgery were used as normal controls. The femur specimens were postoperatively harvested at 4 and 8 weeks for gross, micro-CT, and histological evaluations. The efficacy of PEGDA/ECM/Hon scaffold on the release of proinflammatory cytokines from the macrophages stimulated by lipopolysaccharide (LPS) was evaluated in-vitro.. In vitro results determined that PEGDA/ECM/Hon scaffold could suppress the release of proinflammatory cytokines from macrophages that were stimulated by LPS. Macroscopic images showed that the PEGDA/ECM/Hon group had significantly higher ICRS scoring than that of defect and PEGDA/ECM groups. Micro-CT evaluation demonstrated that much more bony tissue was formed in the defect sites implanted with the PEGDA/ECM scaffold or PEGDA/ECM/Hon scaffold compared with the untreated defects. Histological analysis showed that the PEGDA/ECM/Hon group had a significant enhancement in osteochondral regeneration at 4 and 8 weeks after surgery in comparison with the ECM/PEGDA or defect group.. This study demonstrated that 3D printing of PEGDA/ECM hydrogel incorporating the anti-inflammatory phytomolecule honokiol could provide a promising scaffold for osteochondral defect repair.

    Topics: Animals; Anti-Inflammatory Agents; Biphenyl Compounds; Cartilage, Articular; Extracellular Matrix; Hydrogels; Lignans; Osteoarthritis; Polyethylene Glycols; Printing, Three-Dimensional; Rats; Rats, Sprague-Dawley; Regeneration; Tissue Scaffolds

2020
Schisandrin B ameliorated chondrocytes inflammation and osteoarthritis via suppression of NF-κB and MAPK signal pathways.
    Drug design, development and therapy, 2018, Volume: 12

    Osteoarthritis (OA) is the most prevalent joint disorder in the elderly population, and inflammatory mediators like IL-1β were thought to play central roles in its development. Schisandrin B, the main active component derived from. In the present study, the protective effect and the underlying mechanism of Schisan-drin B on OA was investigated in vivo and in vitro.. The results showed that Schisandrin B decreased IL-1β-induced upregulation of matrix metalloproteinase 3 (MMP3), MMP13, IL-6, and inducible nitric oxide synthase (iNOS) and increased IL-1β-induced downregulation of collagen II, aggrecan, and sox9 as well. Schisandrin B significantly decreased IL-1β-induced p65 phosphorylation and nuclear translocation of p65 in rat chondrocytes. Mitogen-activated protein kinase (MAPK) activation was also inhibited by Schisandrin B, as evidenced by the reduction of p38, extracellular signal-regulated kinase (Erk), and c-Jun amino-terminal kinase (Jnk) phosphorylation. In addition, Schisandrin B prevented cartilage degeneration in rat OA model with significantly lower Mankin's score than the control group.. Our study demonstrated that Schisandrin B ameliorated chondrocytes inflammation and OA via suppression of nuclear factor-κB (NF-κB) and MAPK signal pathways, indicating a therapeutic potential in OA treatment.

    Topics: Animals; Anti-Inflammatory Agents; Cell Survival; Cells, Cultured; Chondrocytes; Cyclooctanes; Dose-Response Relationship, Drug; Inflammation; Lignans; MAP Kinase Signaling System; Matrix Metalloproteinases; NF-kappa B; Osteoarthritis; Polycyclic Compounds; Rats; Rats, Sprague-Dawley; Schisandra; Structure-Activity Relationship

2018
Schisantherin A suppresses interleukin-1β-induced inflammation in human chondrocytes via inhibition of NF-κB and MAPKs activation.
    European journal of pharmacology, 2016, Jun-05, Volume: 780

    Osteoarthritis is a degenerative joint disease that is characterized by the inflammation of synovium. Schisantherin A (SchA), a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra sphenanthera, has been shown to have anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects of SchA on interleukin-1β (IL-1β)-stimulated human osteoarthritis chondrocytes. Human osteoarthritis chondrocytes were pretreated with SchA 1h before IL-1β treatment. The effects of SchA on NO, PGE2, iNOS, COX-2, and TNF-α production were detected in this study. The production of MMP-1, MMP3, MMP13 were measured by ELISA. The expression of NF-κB and MAPKs were detected by western blotting. Our results showed that SchA inhibited IL-1β-induced NO, PGE2, and TNF-α production in a dose-dependent manner. Moreover, IL-1β-induced MMP1, MMP3, and MMP13 expression were significantly inhibited by treatment of SchA. In addition, SchA significantly inhibited IL-1β-induced NF-κB and MAPKs activation. Taken together, these results suggest that SchA exhibits anti-inflammatory effects against IL-1β-stimulated chondrocytes by blocking NF-κB and MAPKs signaling pathways.

    Topics: Anti-Inflammatory Agents, Non-Steroidal; Cell Survival; Chondrocytes; Cyclooctanes; Cyclooxygenase 2; Dinoprostone; Dioxoles; Enzyme Activation; Humans; Interleukin-1beta; Lignans; Matrix Metalloproteinases; Middle Aged; Mitogen-Activated Protein Kinases; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Osteoarthritis; Tumor Necrosis Factor-alpha

2016
Chondroprotective potential of Phyllanthus amarus Schum. & Thonn. in experimentally induced cartilage degradation in the explants culture model.
    In vitro cellular & developmental biology. Animal, 2015, Volume: 51, Issue:4

    Phyllanthus amarus Schum. & Thonn. (P. amarus) has been reported to exhibit anti-inflammation and antiarthritis properties leading to our interest to examine its beneficial effect in osteoarthritis. Thus, this study aimed to explore the chondroprotective potential of P. amarus extract (PAE) and its major compounds, phyllanthin and hypophyllanthin, in a cartilage explant model. Various concentrations of P. amarus extract, phyllanthin and hypophyllanthin, were treated on porcine articular cartilage explants induced with 25 ng/ml of interleukin-1 beta (IL-1β). After 4 days of incubation, the culture medium was measured for the release of sulfate glycosaminoglycans (s-GAGs) and matrix metalloproteinase-2 (MMP-2) activity by DMMB binding assay and zymography, respectively. The explant tissues were analyzed for the remaining of uronic acid content by colorimetric assay and stained with safranin-O for investigation of proteoglycan content. Cell viability of this model was evaluated by lactate dehydrogenase (LDH) assay. Chondroprotective potential of PAE and the major components against IL-1β-induced cartilage explant degradation were revealed by the decreased s-GAGs level and MMP-2 activity in culture medium consistent with an increase in uronic acid and proteoglycan contents in the explants when compared to the IL-1β treatment. These results agreed with those of diacerein and sesamin which used as positive controls. In addition, better chondroprotective activities of P. amarus crude extracts than those of the purified components were disclosed in this study. Hence, this is a pioneering study presenting the chondroprotective potential of PAE which may augment its application for therapeutic use as an antiarthritic agent.

    Topics: Animals; Cartilage, Articular; Culture Media; Glycosaminoglycans; Interleukin-1beta; L-Lactate Dehydrogenase; Lignans; Matrix Metalloproteinase 2; Organ Culture Techniques; Osteoarthritis; Phyllanthus; Plants, Medicinal; Protective Agents; Proteoglycans; Swine; Uronic Acids

2015
Honokiol, a low molecular weight natural product, prevents inflammatory response and cartilage matrix degradation in human osteoarthritis chondrocytes.
    Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2014, Volume: 32, Issue:4

    Proinflammatory cytokine interleukin-1β (IL-1β) stimulates several mediators of cartilage degradation and plays an important role in the pathogenesis of osteoarthritis (OA). Honokiol, a low molecular weight natural product isolated from the Magnolia officinalis, has been shown to possess anti-inflammatory effect. Here, we used an in vitro model of cartilage inflammation to investigate the therapeutic potential of honokiol in OA. Human OA chondrocytes were cultured and pretreated with honokiol (2.5-10 µM) with or without IL-1β (10 ng/ml). Nitric oxide (NO) production was quantified by Griess reagent. Prostaglandin (PG)E2 , metalloproteinase-13 (MMP-13), and interleukin-6 (IL-6) productions were quantified by enzyme-linked immunosorbent assay. The expressions of collagen II, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nuclear factor κB (NF-κB)-related signaling molecules were determined by Western blotting. Our data showed that IL-1β markedly stimulated the expressions of iNOS and COX-2 and the productions of NO, PGE2 , and IL-6, which could be significantly reversed by honokiol. Honokiol could also suppress the IL-1β-triggered activation of IKK/IκBα/NF-κB signaling pathway. Moreover, honokiol significantly inhibited the IL-1β-induced MMP-13 production and collagen II reduction. Taken together, the present study suggests that honokiol may have a chondroprotective effect and may be a potential therapeutic choice in the treatment of OA patients.

    Topics: Aged; Anti-Inflammatory Agents; Biphenyl Compounds; Cell Survival; Chondrocytes; Collagen Type II; Drugs, Chinese Herbal; Humans; I-kappa B Kinase; Lignans; Magnolia; Matrix Metalloproteinase 13; Middle Aged; NF-kappa B; Osteoarthritis; Signal Transduction

2014
Chondroprotective and anti-inflammatory effects of sesamin.
    Phytochemistry, 2012, Volume: 80

    Osteoarthritis (OA) is a major disability of elderly people. Sesamin is the main compound in Sesamun indicum Linn., and it has an anti-inflammatory effect by specifically inhibiting Δ5-desaturase in polyunsaturated fatty acid biosynthesis. The chondroprotective effects of sesamin were thus studied in a porcine cartilage explant induced with interleukin-1beta (IL-1β) and in a papain-induced osteoarthritis rat model. With the porcine cartilage explant, IL-1β induced release of sulfated-glycosaminoglycan (s-GAG) and hydroxyproline release, and this induction was significantly inhibited by sesamin. This ability to inhibit these processes might be due to its ability to decrease expression of MMP-1, -3 and -13, which can degrade both PGs and type II collagen, both at the mRNA and protein levels. Interestingly, activation of MMP-3 might also be inhibited by sesamin. Moreover, in human articular chondrocytes (HACs), some pathways of IL-1β signal transduction were inhibited by sesamin: p38 and JNK. In the papain-induced OA rat model, sesamin treatment reversed the following pathological changes in OA cartilage: reduced disorganization of chondrocytes in cartilage, increased cartilage thickness, and decreased type II collagen and PGs loss. Sesamin alone might increase formation of type II collagen and PGs in the cartilage tissue of control rats. These results demonstrate that sesamin efficiently suppressed the pathological processes in an OA model. Thus, sesamin could be a potential therapeutic strategy for treatment of OA.

    Topics: Animals; Anti-Inflammatory Agents; Cartilage; Chondrocytes; Collagen Type II; Dioxoles; Dose-Response Relationship, Drug; Gene Expression Regulation, Enzymologic; Glycosaminoglycans; Humans; Hydroxyproline; Interleukin-1beta; JNK Mitogen-Activated Protein Kinases; Lignans; MAP Kinase Signaling System; Matrix Metalloproteinases; Osteoarthritis; p38 Mitogen-Activated Protein Kinases; Papain; Phosphorylation; Proteoglycans; Rats; Swine

2012