Scholarlink

<p>Male infertility is linked to chronic psychological stress, however, the mechanisms underlying chronic stress-induced oligoasthenozoospermia (OAZS) remain incompletely elucidated. Here, we establish a chronic forced swim stress (CFSS) rat model and identify a gut microbiota-testis/epididymis axis as the mediator. CFSS activates the HPA axis, leading to elevated corticosterone levels. The&#xa0;excessed&#xa0;glucocorticoid compromises gut barrier integrity via glucocorticoid receptor signaling, resulting in depletion of <i>Lactobacillus</i> and disruption of vitamins A/E metabolism. These deficits promote upregulation of <i>Sting1</i>. Concurrently, epididymal transcriptomics analysis reveals downregulation of <i>Slc9c2</i> as the basis for impaired sperm motility. Notably, restoration of <i>Lactobacillus</i> and dietary supplementation with vitamins A/E ameliorate OAZS phenotypes. Genetic targeting <i>Sting1</i>/<i>Slc9c2</i> in CFSS model rats treated with vitamins A/E, validating the involvement of vitamin A/E metabolism-<i>Sting1</i>/<i>Slc9c2</i> axis in mediating CFSS-induced OAZS. These findings redefines OAZS as a multisystem disorder driven by gut microbial-metabolic-testis/epididymis axis dysregulation and proposes microbiota-targeted therapies for chronic stress-induced infertility.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Chronic stress drives oligoasthenozoospermia via gut microbiota-vitamin-Sting1/Slc9c2 axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月8日

查看全文
  • Jia-Chen Zheng,
  • Zi-Run Jin,
  • Bo-Heng Liu,
  • Yue Tian,
  • Jia-Xing Li,
  • Jie Cai,
  • Hui Jiang,
  • Guo-Gang Xing

摘要

Male infertility is linked to chronic psychological stress, however, the mechanisms underlying chronic stress-induced oligoasthenozoospermia (OAZS) remain incompletely elucidated. Here, we establish a chronic forced swim stress (CFSS) rat model and identify a gut microbiota-testis/epididymis axis as the mediator. CFSS activates the HPA axis, leading to elevated corticosterone levels. The excessed glucocorticoid compromises gut barrier integrity via glucocorticoid receptor signaling, resulting in depletion of Lactobacillus and disruption of vitamins A/E metabolism. These deficits promote upregulation of Sting1. Concurrently, epididymal transcriptomics analysis reveals downregulation of Slc9c2 as the basis for impaired sperm motility. Notably, restoration of Lactobacillus and dietary supplementation with vitamins A/E ameliorate OAZS phenotypes. Genetic targeting Sting1/Slc9c2 in CFSS model rats treated with vitamins A/E, validating the involvement of vitamin A/E metabolism-Sting1/Slc9c2 axis in mediating CFSS-induced OAZS. These findings redefines OAZS as a multisystem disorder driven by gut microbial-metabolic-testis/epididymis axis dysregulation and proposes microbiota-targeted therapies for chronic stress-induced infertility.