ArticleFood & nutrition research2025
Evaluation of the anti-osteoarthritic effects and mechanisms of
Article in Food & nutrition research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Effects of Acupuncture at ST36 and SP6 on Activity Levels and Pain Thresholds Through Interleukin-1, Interleukin-6, Cortisol, and Matrix Metalloproteinase-13 Modulation in an Osteoarthritis Rat Model.Journal of pharmacopuncture · 2026Article
- Exploring the Role ofOrthopedic research and reviews · 2026Review
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Authors and funding
5 authors.
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Abstract
Background: Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage degradation, subchondral bone erosion, and chronic inflammation. Current treatments primarily focus on symptom relief and have significant side effects, highlighting the need for safer, more effective alternatives. Objective: This study aimed to investigate the anti-osteoarthritic effects and mechanisms of action of CQE in a monosodium iodoacetate (MIA)-induced OA rat model. Design: Sprague-Dawley (SD) rats were induced with OA through intra-articular injection of MIA and treated with CQE at doses of 30, 50, and 100 mg/kg body weight (BW)/day. The effects of CQE on knee joint damage, subchondral bone erosion, cartilage structure, proteoglycan content, and the expression of inflammatory mediators and matrix metalloproteinases (MMPs) were assessed using micro-computed tomography (micro-CT), histological staining, immunofluorescence, and real-time reverse transcription-polymerase chain reaction (RT-PCR). Results: CQE significantly mitigated knee joint damage, reduced subchondral bone erosion, and enhanced bone volume and trabecular structure in MIA-induced OA rats. It also preserved cartilage integrity by maintaining proteoglycan content and the expression of collagen type II alpha 1 (COL2A1) and aggrecan. Moreover, CQE suppressed the mRNA expression of inflammatory mediators [inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and 5-lipoxygenase (5-LOX)], pro-inflammatory cytokines [interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)], and MMPs (MMP-2, MMP-3, MMP-9, and MMP-13), indicating strong anti-inflammatory and cartilage-protective effects. Conclusions: CQE exhibits significant therapeutic potential in managing OA by targeting multiple aspects of disease progression, including inflammation, cartilage degradation, and bone erosion. Further research is needed to explore long-term efficacy, safety, and the molecular mechanisms of CQE, as well as to validate these findings in human clinical trials.
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