ArticleMolecular biology reports2025
Lycium barbarum polysaccharide alleviates osteoarthritis progression in mice DMM model by inhibiting chondrocytes ferroptosis and promoting the gut Lactobacillus/Alistipes ratio.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Anti-Osteoarthritis Effect of Medicinal and Edible Homologous Bioactive Components and Chinese Medicinal and Health Food Varieties.Nutrients · 2026Review
- Ferroptosis-Driven Senescence Loop as a Central Amplifier of Osteoarthritis Progression.Biomolecules & therapeutics · 2026Review
- "Gut-Joint Axis" Perspective on Immunometabolic Crosstalk in Osteoarthritis: A Narrative Review of Mechanistic Insights and Targeted Strategies.Journal of inflammation research · 2026Review
- Mechanistic insights into gut microbiota dysbiosis in osteoarthritis based on the gut-joint axis.Frontiers in immunology · 2026Review
- Research progress on the mechanism of chondrocyte ferroptosis in osteoarthritis.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundLycium barbarum polysaccharides (LBP) are natural polysaccharides compounds with multiple biological activities. Both ferroptosis, a form of cell death, and gut microbiota are involved in the pathological process of osteoarthritis (OA). The effects and mechanisms of LBP on chondrocyte ferroptosis, gut microbiota, and cartilage degradation are still unclear.
methodsWe evaluated the effects of LBP on cell activity through CCK8 assay. Iron ion content assay, iron staining, lipid peroxidation probe C11-BODIPY assay, malondialdehyde (MDA) assay and glutathione (GSH) content assay were used to evaluate the degree of ferroptosis. Ferroptosis-related proteins were tested by Western blot and immunofluorescence. The protective effect of LBP on cartilage damage and gut microbiota/metabolome was evaluated in the destabilization of medial meniscus (DMM)-induced OA model of mice.
resultsLBP reversed Erastin-induced ferroptosis and the effects of Erastin/IL-1β on chondrocyte anabolic/catabolic metabolism. LBP reduced the protein level of KEAP1 and increased the protein level of Nrf2 in chondrocytes. In DMM model, LBP significantly alleviated the pathological process of cartilage damage, and promoted the gut Lactobacillus/Alistipes ratio.
conclusionLBP alleviates OA in DMM model mice by inhibiting chondrocytes ferroptosis and promoting the gut Lactobacillus/Alistipes ratio, suggesting LBP as a promising therapeutic approach for OA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.