ArticlePloS one2016
Glucosamine Downregulates the IL-1β-Induced Expression of Proinflammatory Cytokine Genes in Human Synovial MH7A Cells by O-GlcNAc Modification-Dependent and -Independent Mechanisms.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04661267 (A Randomized, Double-Blind, Placebo-Controlled Trial of Regenexx Stem Cell Support Formula), which is not on this map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Randomized, Double-Blind, Placebo-Controlled Trial of Regenexx Stem Cell Support Formula
Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Exploring the drug repurposing potential of lisinopril against TNBS-induced colitis in Wistar rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- O-GlcNAcylation: Sagacious Orchestrator of Bone-, Joint-, and Spine-Related Diseases.Journal of proteome research · 2025Review
- O-GlcNAcylation: roles and potential therapeutic target for bone pathophysiology.Cell communication and signaling : CCS · 2024Review
- Association between genetically proxied glucosamine and risk of cancer and non-neoplastic disease: A Mendelian randomization study.Frontiers in genetics · 2024Article
- The role of O-GlcNAcylation in bone metabolic diseases.Frontiers in physiology · 2024Review
- Effects of Modified Glucosamine on the Chondrogenic Potential of Circulating Stem Cells under Experimental Inflammation.International journal of molecular sciences · 2023Article
- Review
- Targeting ProteinCells · 2022Review
- Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model.Frontiers in immunology · 2022Article
- Effects of isoflavone derivatives on the production of inflammatory cytokines by synovial cells.Experimental and therapeutic medicine · 2021Article
- Antcin K Inhibits TNF-α, IL-1β and IL-8 Expression in Synovial Fibroblasts and Ameliorates Cartilage Degradation: Implications for the Treatment of Rheumatoid Arthritis.Frontiers in immunology · 2021Article
- Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells.Biochemistry and biophysics reports · 2019Article
- O-GlcNAcylation in immunity and inflammation: An intricate system (Review).International journal of molecular medicine · 2019Review
- NLRP3 inflammasome activation by estrogen promotes the progression of human endometrial cancer.OncoTargets and therapy · 2019Article
- Glucosamine prevents polarization of cytotoxic granules in NK-92 cells by disturbing FOXO1/ERK/paxillin phosphorylation.PloS one · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is one of the major joint diseases, and the synovial inflammation is involved in the pathogenesis and progression of OA. Glucosamine (GlcN) is widely used as a dietary supplement for OA, and is expected to exert the antiinflammatory action in OA. However, the detailed mechanism for the antiinflammatory action of GlcN remains poorly understood. In this study, to elucidate the molecular mechanism involved in the GlcN-medicated regulation of synovial cell activation, we comprehensively analyzed the effect of GlcN on the gene expression using a human synovial cell line MH7A by DNA microarray. The results indicated that GlcN significantly downregulates the expression of 187 genes (≤1/1.5-fold) and upregulates the expression of 194 genes (≥1.5-fold) in IL-1β-stimulated MH7A cells. Interestingly, pathway analysis indicated that among the 10 pathways into which the GlcN-regulated genes are categorized, the 4 pathways are immune-related. Furthermore, GlcN suppressed the expression of proinflammatory cytokine genes (such as IL-6, IL-8, IL-24 and TNF-α genes). In addition, GlcN-mediated O-GlcNAc modification was involved in the downregulation of TNF-α and IL-8 genes but not IL-6 and IL-24 genes, based on the effects of alloxan, an O-GlcNAc transferase inhibitor. Thus, GlcN likely exerts an antiinflammatroy action in OA by suppressing the expression of proinflammatory cytokine genes in synovial MH7A cells by O-GlcNAc modification-dependent and -independent mechanisms.
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