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<p>Chitosan–astaxanthin nanoparticles (CS–ASTNPs) exhibited an anti-colitis activity, but their poor mobility restricts anti-inflammatory efficacy. <i>Chlamydomonas reinhardtii</i> (<i>C. reinhardtii</i>) was employed to load CS–ASTNPs to construct astaxanthin-loaded microalgal motors (CS–AST@CR). The particle size of CS–AST@CR was 4.2 ± 0.21&#xa0;μm and its swimming speed was 89.3 ± 4.4&#xa0;µm/s, which was slower than native <i>C. reinhardtii</i> (117.2 ± 2.7&#xa0;µm/s), though their movement trajectories remained comparable. Compared to CS–ASTNPs, CS–AST@CR notably alleviated chronic colitis symptoms. It enhanced colon barrier function by promoting ZO-1, occludin, and MUC2 expression. Furthermore, CS–AST@CR markedly reduced TNF-α, IL-1β, and NLRP3 inflammasome production while increasing IL-10 levels. The oxidative response was effectively suppressed via activating the Nrf2/HO-1 pathway. Additionally, CS–AST@CR significantly increased <i>Lactobacillus</i> and <i>Enterorhabdus</i> abundance; whereas, CS–ASTNPs elevated <i>Akkermansia</i> and <i>Bifidobacteriaceae</i> richness. Collectively, CS–AST@CR integrated the advantages of microalgal motility and nanoparticle functionality, showing great potential for development as functional foods or therapeutic agents for colitis treatment.</p>

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Constructing of astaxanthin-loaded microalgal motor and its effect on ameliorating chronic colitis involving in oxidative stress, gut microbiota, and intestinal barrier

  • 期刊论文

  • 发表日期：

    2026年7月28日

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  • Hongyan Li,
  • Xinwei Gong,
  • Huiru Li,
  • Chuqiao Zhang,
  • Lu Yang,
  • Hongxia Che,
  • Yuchao Gu

摘要

Chitosan–astaxanthin nanoparticles (CS–ASTNPs) exhibited an anti-colitis activity, but their poor mobility restricts anti-inflammatory efficacy. Chlamydomonas reinhardtii (C. reinhardtii) was employed to load CS–ASTNPs to construct astaxanthin-loaded microalgal motors (CS–AST@CR). The particle size of CS–AST@CR was 4.2 ± 0.21 μm and its swimming speed was 89.3 ± 4.4 µm/s, which was slower than native C. reinhardtii (117.2 ± 2.7 µm/s), though their movement trajectories remained comparable. Compared to CS–ASTNPs, CS–AST@CR notably alleviated chronic colitis symptoms. It enhanced colon barrier function by promoting ZO-1, occludin, and MUC2 expression. Furthermore, CS–AST@CR markedly reduced TNF-α, IL-1β, and NLRP3 inflammasome production while increasing IL-10 levels. The oxidative response was effectively suppressed via activating the Nrf2/HO-1 pathway. Additionally, CS–AST@CR significantly increased Lactobacillus and Enterorhabdus abundance; whereas, CS–ASTNPs elevated Akkermansia and Bifidobacteriaceae richness. Collectively, CS–AST@CR integrated the advantages of microalgal motility and nanoparticle functionality, showing great potential for development as functional foods or therapeutic agents for colitis treatment.