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Triptolide exposure triggers ovarian inflammation by activating cGAS-STING pathway and decrease oocyte quality in

Si-Yao Cheng1, Yi-Fan Yang1, Ya-Long Wang2

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Triptolide (TPL) causes ovarian damage by affecting mitochondrial function and activating inflammation pathways. This leads to reduced fertility and oocyte quality, hindering follicular development.

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Area of Science:

  • Toxicology
  • Reproductive Biology
  • Molecular Biology

Background:

  • Triptolide (TPL), from Tripterygium wilfordii, has anti-tumor and anti-immune uses.
  • TPL causes multiorgan toxicity, including female reproductive system damage.
  • Mechanisms of TPL-induced ovarian damage are not well understood.

Purpose of the Study:

  • Investigate the mechanisms of TPL-induced ovarian toxicity.
  • Evaluate the impact of TPL on ovarian function and oocyte quality.
  • Identify molecular pathways involved in TPL's reproductive side effects.

Main Methods:

  • Mouse toxicological model for TPL exposure.
  • Assessment of ovarian coefficient and fertility.
  • Analysis of mitochondrial function, mtDNA release, and cGAS-STING pathway activation.
  • Evaluation of oocyte meiotic maturation, spindle, and MTOC morphology.
  • Reduced representation bisulfite sequencing (RRBS) for confirmation.

Main Results:

  • TPL exposure decreased ovarian coefficient and fertility in mice.
  • TPL disrupted mitochondrial function, leading to mtDNA release and cGAS-STING pathway activation.
  • Ovarian inflammation and follicular development hindrance were observed.
  • TPL impaired oocyte meiotic maturation, affecting spindle and MTOCs.

Conclusions:

  • TPL induces ovarian damage through mitochondrial dysfunction and inflammatory pathways.
  • Impaired follicular development and reduced oocyte quality are key consequences of TPL exposure.
  • Understanding these mechanisms is crucial for managing TPL's reproductive toxicity.