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<p><i>Schistosoma mansoni</i> is a major cause of schistosomiasis, a neglected tropical disease that induces granulomatous inflammation, fibrosis, and liver damage.&#xa0;Fucoidan (FUC), a sulfated polysaccharide from brown seaweed, was evaluated for its anti-helminthic, anti-inflammatory, and antifibrotic effects against immature stages of&#xa0;<i>S. mansoni</i>&#xa0;in mice. Forty-eight CD-1 Swiss male albino mice were infected and allocated into six groups: infected untreated control, praziquantel-treated, and FUC-treated groups at 7, 21, 35, and 42&#xa0;days post-infection. Treatment with FUC at 7, 21, and 35 dpi significantly reduced worm burden, granuloma size, fibrosis, and the expression of TNF-α, IL-1β, and iNOS in liver tissue.&#xa0;The strongest antipathological effects were observed with early-to-mid treatment, particularly FUC7, FUC21, and FUC35.&#xa0;In contrast, FUC42 showed weaker benefit, indicating that efficacy is timing-dependent. These findings suggest that FUC may be a promising candidate for early intervention in&#xa0;<i>S. mansoni</i>&#xa0;infection.</p>

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In vivo assessment of anti-helminthic and anti-inflammatory effects of Fucoidan on Schistosoma mansoni immature stages

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月17日

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  • Suzan H. Elgendy,
  • Wafaa A. Aboukamar,
  • Marwa M. Hamouda,
  • Amira Ismail,
  • Rehab T. Eldesoky,
  • Ayat A. Elblihy

摘要

Schistosoma mansoni is a major cause of schistosomiasis, a neglected tropical disease that induces granulomatous inflammation, fibrosis, and liver damage. Fucoidan (FUC), a sulfated polysaccharide from brown seaweed, was evaluated for its anti-helminthic, anti-inflammatory, and antifibrotic effects against immature stages of S. mansoni in mice. Forty-eight CD-1 Swiss male albino mice were infected and allocated into six groups: infected untreated control, praziquantel-treated, and FUC-treated groups at 7, 21, 35, and 42 days post-infection. Treatment with FUC at 7, 21, and 35 dpi significantly reduced worm burden, granuloma size, fibrosis, and the expression of TNF-α, IL-1β, and iNOS in liver tissue. The strongest antipathological effects were observed with early-to-mid treatment, particularly FUC7, FUC21, and FUC35. In contrast, FUC42 showed weaker benefit, indicating that efficacy is timing-dependent. These findings suggest that FUC may be a promising candidate for early intervention in S. mansoni infection.