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<p>Nutritional interventions, including Royal Jelly (RJ), are potential modulators of tissue function during aging. However, the molecular mechanisms underlying food-derived modulation of tissue physiology remain poorly understood. Here we show that dietary RJ enhances stem/progenitor cell activity with age- and tissue-dependent <i>Chi3l1</i>-mediated increases in CD206-positive macrophages. In aged mice, RJ administration increased proliferative activity of stem/progenitor cells in the skin and brain, accompanied by improved hair phenotypes and enhanced neurogenesis. Transcriptomic screening in human mesenchymal stem/stromal cells identified <i>CHI3L1</i> as an RJ-responsive gene that is downregulated during cellular senescence. Hepatocyte-specific disruption of <i>Chi3l1</i> using adeno-associated virus-mediated gene editing demonstrated that <i>Chi3l1</i> is required for maintaining hepatic CD206-positive macrophage populations in vivo. Similar effects were observed with 10-hydroxy-2-decenoic acid, a major RJ component. These findings suggest that <i>Chi3l1</i> is a physiologically regulated immune mediator, rather than a pathogenic factor in disease contexts, highlighting the importance of mechanistic studies of food-derived biological effects.</p>

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Royal jelly ameliorates age-associated stem cell dysfunction with Chi3l1-mediated increase in CD206-positive macrophages

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月24日

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  • Yukie Kande,
  • Yasuaki Ikuno,
  • Ayano Narumoto,
  • Kahori Minami,
  • Kasumi Nobuhiro,
  • Koichiro Watanabe,
  • Dai Ihara,
  • Manabu Shirai,
  • Noriki Fujimoto,
  • Nobuaki Okumura,
  • Hayato Naka-Kaneda

摘要

Nutritional interventions, including Royal Jelly (RJ), are potential modulators of tissue function during aging. However, the molecular mechanisms underlying food-derived modulation of tissue physiology remain poorly understood. Here we show that dietary RJ enhances stem/progenitor cell activity with age- and tissue-dependent Chi3l1-mediated increases in CD206-positive macrophages. In aged mice, RJ administration increased proliferative activity of stem/progenitor cells in the skin and brain, accompanied by improved hair phenotypes and enhanced neurogenesis. Transcriptomic screening in human mesenchymal stem/stromal cells identified CHI3L1 as an RJ-responsive gene that is downregulated during cellular senescence. Hepatocyte-specific disruption of Chi3l1 using adeno-associated virus-mediated gene editing demonstrated that Chi3l1 is required for maintaining hepatic CD206-positive macrophage populations in vivo. Similar effects were observed with 10-hydroxy-2-decenoic acid, a major RJ component. These findings suggest that Chi3l1 is a physiologically regulated immune mediator, rather than a pathogenic factor in disease contexts, highlighting the importance of mechanistic studies of food-derived biological effects.