Protective effects ROS up-regulation on premature ovarian failure by suppressing ROS-TERT signal pathway

H-L Jiang1, L-Q Cao, H-Y Chen

  • 1Department of Obstetrics, The Fifth Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China. ganyapingya@163.com.

Abstract

Insights

Reactive oxygen species (ROS) elevate in premature ovarian failure (POF), inhibiting telomerase reverse transcriptase (TERT) and worsening the condition. Targeting the ROS-TERT pathway may offer a new treatment for POF.

Area of Science:

  • Gynecology
  • Reproductive Biology
  • Cellular Biology

Background:

  • Premature ovarian failure (POF) is a gynecological condition with unclear pathogenic mechanisms.
  • Decreased telomerase reverse transcriptase (TERT) activity has been observed in POF.
  • The role of oxidative stress, a suppressor of TERT, in POF remains understudied.

Purpose of the Study:

  • To investigate the involvement of reactive oxygen species (ROS) and TERT in the pathogenesis of POF.
  • To explore the potential of targeting the ROS-TERT pathway for POF treatment.

Main Methods:

  • A rat model of POF was established using cyclophosphamide and busulfan.
  • Hormone levels (FSH, inhibin B) and ovarian histology were assessed.
  • Western blot was used to measure TERT expression.
  • N-acetyl-cysteine (NAC) was used to reduce ROS, and TERT small interfering RNA (siRNA) was used to suppress TERT.

Main Results:

  • POF models exhibited ovarian atrophy, reduced follicles, increased follicular atresia, and elevated FSH and decreased inhibin B levels.
  • Elevated ROS and decreased TERT levels were observed in POF rats.
  • NAC treatment reduced ROS and increased TERT expression, ameliorating POF.
  • TERT siRNA exacerbated the POF condition.

Conclusions:

  • Increased ROS inhibits TERT expression and activity, contributing to POF.
  • The ROS-TERT pathway is implicated in POF pathogenesis.
  • Modulating the ROS-TERT pathway presents a potential therapeutic strategy for POF.

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