关键词: inflammatory oligo-fucoidan-based formula osteoarthritis oxidative stress

Mesh : Animals Mice Cartilage, Articular / drug effects pathology Cyclooxygenase 2 / metabolism Disease Models, Animal Iodoacetates Iodoacetic Acid Nitric Oxide Synthase Type II / antagonists & inhibitors metabolism Osteoarthritis / drug therapy chemically induced Oxidative Stress / drug effects Polysaccharides / pharmacology Rats Cyclooxygenase 2 Inhibitors / chemistry pharmacology

来  源:   DOI:10.3390/md22050211   PDF(Pubmed)

Abstract:
Osteoarthritis (OA) is a debilitating joint disorder characterized by cartilage degradation and chronic inflammation, accompanied by high oxidative stress. In this study, we utilized the monosodium iodoacetate (MIA)-induced OA model to investigate the efficacy of oligo-fucoidan-based formula (FF) intervention in mitigating OA progression. Through its capacity to alleviate joint bearing function and inflammation, improvements in cartilage integrity following oligo-fucoidan-based formula intervention were observed, highlighting its protective effects against cartilage degeneration and structural damage. Furthermore, the oligo-fucoidan-based formula modulated the p38 signaling pathway, along with downregulating cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, contributing to its beneficial effects. Our study provides valuable insights into targeted interventions for OA management and calls for further clinical investigations to validate these preclinical findings and to explore the translational potential of an oligo-fucoidan-based formula in human OA patients.
摘要:
骨关节炎(OA)是一种以软骨退化和慢性炎症为特征的衰弱性关节疾病,伴有高氧化应激。在这项研究中,我们利用碘乙酸钠(MIA)诱导的OA模型研究了基于低聚岩藻依聚糖的配方(FF)干预在缓解OA进展方面的疗效.通过其减轻关节轴承功能和炎症的能力,观察到基于低聚岩藻聚糖的配方干预后软骨完整性的改善,强调其对软骨退化和结构损伤的保护作用。此外,基于寡岩藻聚糖的配方调节p38信号通路,随着环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)的表达下调,有助于其有益效果。我们的研究为OA管理的针对性干预提供了有价值的见解,并呼吁进一步的临床研究以验证这些临床前发现,并探索基于寡岩藻依聚糖的配方在人类OA患者中的转化潜力。
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