ArticleJournal of cellular and molecular medicine2025
Effects of Different Doses of Glucosamine Hydrochloride on Cartilage Tissue and Levels of Joint Injury Markers in Knee Osteoarthritis.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Serum Omentin-1 and CS846: Biomarkers for diagnosis and post-TKA functional outcomes in knee osteoarthritis.Journal of medical biochemistry · 2026Article
- Impact of Symptomatic Slow-Acting Drugs on Inflammatory Pathways in Osteoarthritis: Therapeutic Advances and Future Challenges.ACS pharmacology & translational science · 2025Review
- A Compartmentalized Joint-on-chip (JoC) Model to Unravel the Contribution of Cartilage and Synovium to Osteoarthritis Pathogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Effects of celecoxib combined with glucosamine hydrochloride in the management of knee osteoarthritis.American journal of translational research · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study analysed the effects of different doses of glucosamine hydrochloride (GS-HCl) on cartilage tissue and the levels of joint injury markers in knee osteoarthritis (KOA). The Sham group, KOA group, low-dose GS-HCl group and high-dose GS-HCl group were established, with six mice in each group. The levels of joint injury markers (COMP, CS846 and CTX-II), inflammatory cytokines (IL-6, TNF-α and iNOS), oxidative stress indicators (MDA and SOD) and matrix remodelling proteins (MMP-3 and TIMP-1) were analysed. The degeneration of knee femoral condyles, histopathological changes and tissue apoptosis rate of the articular cartilage was also assessed. Mice in the KOA group displayed elevated COMP, CS846, CTX-II, IL-6, TNF-α, iNOS and MDA contents, reduced SOD activity, an irregular articular cartilage surface, a serious cartilage defect, a disordered articular cartilage surface in the defect, disappeared cartilage cells, obvious synovial cell proliferation and visible inflammatory cell infiltration. In the tissue, apoptosis rate and MMP-3 and TIMP-1 protein expression increased. Different doses of GS-HCl treatment could reduce COMP, CS846, CTX-II, IL-6, TNF-α, iNOS and MDA contents, apoptosis rate and MMP-3 and TIMP-1 protein expression, increase SOD activity and improve histopathological conditions in KOA mice. The improvement effects in each indicator in the high dose-GS-HCl group were more significant than those in the low dose-GS-HCl group. The intragastric administration of the GS-HCl group partially prevents the degeneration of articular cartilage in KOA mice. The mechanism may be to reduce inflammatory factors and oxidative stress indicator expression and matrix degradation, thereby delaying osteoarthritis progression.
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Registered trials
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