Low-Molecular-Weight Fucoidan Inhibits the Viability and Invasiveness and Triggers Apoptosis in IL-1β-Treated Human...

Area of Science:

• Marine Biotechnology
• Immunology
• Rheumatology

Background:

• Rheumatoid arthritis (RA) involves inflammation of synovial cells.
• Fibroblast-like synoviocytes (RAFLS) play a crucial role in RA pathogenesis.
• Interleukin-1beta (IL-1β) is a key inflammatory mediator in RA.

Purpose of the Study:

• To investigate the effects of low-molecular-weight (LMW) fucoidan on IL-1β-stimulated RAFLS.
• To determine the molecular mechanisms underlying fucoidan's action in RAFLS.

Main Methods:

• Cell viability and apoptosis assays (MTT, Annexin V/PI).
• Cell invasion assays (Transwell).
• Molecular analyses including RT-PCR, Western blot, ELISA, and EMSA for gene expression, protein secretion, and NF-κB activity.

Main Results:

• LMW fucoidan inhibited IL-1β-induced RAFLS viability and promoted apoptosis.
• Fucoidan reduced RAFLS invasion and secretion of matrix metalloproteinases (MMP-1, MMP-3, MMP-9).
• Fucoidan suppressed NF-κB activation and p38 MAPK phosphorylation in stimulated RAFLS.

Conclusions:

• LMW fucoidan demonstrates anti-proliferative, pro-apoptotic, and anti-invasive effects on IL-1β-stimulated RAFLS.
• These effects are mediated through the inhibition of NF-κB and p38 signaling pathways.
• LMW fucoidan holds potential as a therapeutic agent for rheumatoid arthritis.