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Related Experiment Video

Updated: Sep 11, 2025

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
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Fucoidan Modulates Osteoarthritis Progression Through miR-22/HO-1 Pathway.

Tsung-Hsun Hsieh1,2, Jar-Yi Ho3, Chih-Chien Wang4

  • 1Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114, Taiwan.

Cells
|August 13, 2025
PubMed
Summary
This summary is machine-generated.

Fucoidan protects against osteoarthritis (OA) by reducing oxidative stress and inflammation. It modulates the miR-22/heme oxygenase-1 pathway, offering a potential therapeutic strategy for OA treatment.

Keywords:
chondrocytesfucoidanmiR-22/HO-1 pathwayosteoarthritissynovial fibroblasts

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteoarthritis (OA) is a degenerative joint disease causing significant disability in the elderly.
  • Interleukin-1 beta (IL-1β) plays a key role in OA pathogenesis by inducing articular tissue damage.
  • Fucoidan, a sulfated polysaccharide, possesses anti-inflammatory and antioxidant properties with potential therapeutic applications in OA.

Purpose of the Study:

  • To investigate the protective effects of fucoidan against IL-1β-induced damage in human chondrocytes and synovial fibroblasts.
  • To elucidate the underlying molecular mechanisms, focusing on the role of microRNAs (miRs) and heme oxygenase-1 (HO-1).
  • To validate the findings in an in vivo rat model of OA.

Main Methods:

  • Human chondrocytes and synovial fibroblasts were treated with fucoidan prior to IL-1β stimulation.
  • Oxidative stress markers and catabolic enzyme levels were measured to assess fucoidan's protective effects.
  • An OA rat model was used for in vivo validation.
  • In silico and experimental methods, including luciferase reporter assays, were employed to identify and validate miR-HO-1 interactions.

Main Results:

  • Fucoidan demonstrated protective effects against IL-1β-induced oxidative stress and catabolic processes in vitro and in vivo.
  • Fucoidan treatment normalized HO-1 expression and reduced inducible nitric oxide synthase and matrix metalloproteinase levels.
  • A novel mechanism involving fucoidan's modulation of the miR-22/HO-1 pathway in OA was identified, with miR-22 upregulation by IL-1β and subsequent attenuation by fucoidan.

Conclusions:

  • Fucoidan effectively mitigates OA-related oxidative stress in joint cells via the miR-22/HO-1 axis.
  • The miR-22/HO-1 pathway is a critical therapeutic target for osteoarthritis.
  • Fucoidan represents a promising therapeutic agent for managing osteoarthritis.