Choi Yean-Jung, Jung Jae In, Bae Jaewoo, Lee Jae Kyoung, Kim Eun Ji
Department of Food and Nutrition, Sahmyook University, Seoul, Republic of Korea.
Industry Coupled Cooperation Center for Bio Healthcare Materials, Hallym University, Chuncheon, Republic of Korea.
Food Nutr Res. 2025 Apr 15;69. doi: 10.29219/fnr.v69.12173. eCollection 2025.
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. extract (CQE), containing bioactive flavonoids quercetin and isorhamnetin, has shown potential anti-inflammatory and cartilage-protective properties.
This study aimed to investigate the anti-osteoarthritic effects and mechanisms of action of CQE in a monosodium iodoacetate (MIA)-induced OA rat model.
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).
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.
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.
骨关节炎（OA）是一种退行性关节疾病，其特征为软骨降解、软骨下骨侵蚀和慢性炎症。目前的治疗主要集中于缓解症状且有显著副作用，这凸显了对更安全、更有效替代方案的需求。含有生物活性黄酮类化合物槲皮素和异鼠李素的提取物（CQE）已显示出潜在的抗炎和软骨保护特性。
本研究旨在探讨CQE在碘乙酸钠（MIA）诱导的OA大鼠模型中的抗骨关节炎作用及作用机制。
通过关节内注射MIA诱导Sprague-Dawley（SD）大鼠患OA，并以30、50和100毫克/千克体重（BW）/天的剂量用CQE进行治疗。使用微型计算机断层扫描（micro-CT）、组织学染色、免疫荧光和实时逆转录-聚合酶链反应（RT-PCR）评估CQE对膝关节损伤、软骨下骨侵蚀、软骨结构、蛋白聚糖含量以及炎症介质和基质金属蛋白酶（MMPs）表达的影响。
CQE显著减轻了MIA诱导的OA大鼠的膝关节损伤，减少了软骨下骨侵蚀，并增加了骨体积和小梁结构。它还通过维持蛋白聚糖含量以及Ⅱ型胶原α1（COL2A1）和聚集蛋白聚糖的表达来保持软骨完整性。此外，CQE抑制了炎症介质[诱导型一氧化氮合酶（iNOS）、环氧化酶-2（COX-2）和5-脂氧合酶（5-LOX）]、促炎细胞因子[白细胞介素（IL）-1β、IL-6和肿瘤坏死因子-α（TNF-α）]以及MMPs（MMP-2、MMP-3、MMP-9和MMP-13）的mRNA表达，表明其具有强大的抗炎和软骨保护作用。
CQE通过针对疾病进展的多个方面，包括炎症、软骨降解和骨侵蚀，在治疗OA方面展现出显著的治疗潜力。需要进一步研究以探索CQE的长期疗效、安全性及其分子机制，并在人类临床试验中验证这些发现。
