Fucoxanthin mitigates inflammation and angiogenesis in rheumatoid arthritis via regulation of the PPAR-γ/CTGF pathway
Main Article Content
Keywords
angiogenesis, fucoxanthin, PPAR-γ/CTGF pathway, rheumatoid arthritis
Abstract
Background: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder that causes joint pain and significantly impairs patients’ quality of life. Fucoxanthin, a naturally occurring carotenoid found in seaweeds and diatoms, has been reported to exert various therapeutic effects in multiple pathological conditions. However, its regulatory role in the pathogenesis of RA remains largely undefined.
Methods: Cell viability was assessed using the cell counting kit-8 (CCK-8) assay, while cell migration and invasion were evaluated through the wound healing and Transwell assays, respectively. Angiogenic potential was determined by the tube formation assay. The levels of pro-inflammatory cytokines, including interleukin (IL)-6, IL-1β, and IL-8, were measured using enzyme-linked-immunosorbent serologic assay. Intracellular reactive oxygen species (ROS) levels were analyzed via DCFH-DA staining, and protein expression was evaluated by Western blot analysis.
Results: Fucoxanthin significantly suppressed tumor necrosis factor-α (TNF-α)-induced proliferation of MH7A synovial cells. Additionally, TNF-α stimulation enhanced cell migration and invasion, whereas these effects were reversed with fucoxanthin treatment. TNF-α also promoted angiogenesis, as evidenced by an increased number of tube formations, which were markedly reduced by fucoxanthin in a dose-dependent manner (control; TNF-α; TNF-α + fucoxanthin [2 μM]; and TNF-α + fucoxanthin [4 μM], with respective values of 1.33 ± 0.58; 26 ± 3.61; 17 ± 2.65; and 8.33 ± 1.53; P < 0.001). Moreover, fucoxanthin alleviated TNF-α-induced inflammatory cytokine release and oxidative stress. Mechanistically, fucoxanthin was found to regulate the PPAR-γ/CTGF signaling pathway.
Conclusion: Fucoxanthin may attenuate inflammation and angiogenesis in RA by modulating the PPAR-γ/CTGF pathway, suggesting its potential as a therapeutic agent for managing RA.
References
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