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<p>Premature ovarian insufficiency (POI) threatens women’s reproductive health. Emerging evidence implicates the gut-ovary axis in POI pathogenesis. This study explored the probiotic <i>Lactobacillus salivarius</i> Li01 in a <i>Tripterygium wilfordii</i> glycosides-induced POI mouse model. Li01 effectively mitigated POI progression by restoring hormone levels, increasing functional follicle numbers, and improving ovarian antioxidant function. These beneficial effects were primarily mediated through modulation of the gut microbiota and host tryptophan metabolism. Notably, a tryptophan-enriched diet alone did not improve POI. When combined with Li01, it synergistically amplified the kynurenine pathway. This shift promoted ovarian NAD⁺ production by upregulating the levels of NAMPT, while attenuating NAD⁺ depletion through downregulation of CD38 expression. The elevated NAD⁺ levels subsequently activated SIRT1 expression, stimulated the synthesis of SOD and other antioxidants, and inhibited the Caspase-1/IL‑1β inflammasome axis. These findings highlight Li01 as a potential POI therapy through microbiota-metabolic regulation, offering new mechanistic insights into gut-ovarian interactions.</p><p></p>

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Lactobacillus salivarius li01 alleviates premature ovarian insufficiency via gut microbiota-mediated modulation of tryptophan metabolism

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月8日

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  • Lingnv Yao,
  • Siyuan Xie,
  • Shuobo Zhang,
  • Furong Ba,
  • Huijuan Jing,
  • Bo Qiu,
  • Lvwan Xu,
  • Shengyi Han,
  • Hang Xiao,
  • Ming Zhao,
  • Xiaowei Shi,
  • Lanjuan Li,
  • Mingfei Yao

摘要

Premature ovarian insufficiency (POI) threatens women’s reproductive health. Emerging evidence implicates the gut-ovary axis in POI pathogenesis. This study explored the probiotic Lactobacillus salivarius Li01 in a Tripterygium wilfordii glycosides-induced POI mouse model. Li01 effectively mitigated POI progression by restoring hormone levels, increasing functional follicle numbers, and improving ovarian antioxidant function. These beneficial effects were primarily mediated through modulation of the gut microbiota and host tryptophan metabolism. Notably, a tryptophan-enriched diet alone did not improve POI. When combined with Li01, it synergistically amplified the kynurenine pathway. This shift promoted ovarian NAD⁺ production by upregulating the levels of NAMPT, while attenuating NAD⁺ depletion through downregulation of CD38 expression. The elevated NAD⁺ levels subsequently activated SIRT1 expression, stimulated the synthesis of SOD and other antioxidants, and inhibited the Caspase-1/IL‑1β inflammasome axis. These findings highlight Li01 as a potential POI therapy through microbiota-metabolic regulation, offering new mechanistic insights into gut-ovarian interactions.