Related Experiment Video

Updated: Sep 14, 2025

Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption
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Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption

Published on: July 30, 2016

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Exogenous melatonin alleviates premature ovarian failure by regulating granulosa cell autophagy

Guang-Hu Zhou1,2, Ye-Fei He1, Hai-Ling Wang1

  • 1College of Veterinary Medicine, Northeast Agricultural University, Harbin, PR China.

NPJ Regenerative Medicine
|July 23, 2025
PubMed

Insights

Melatonin (Mel) treatment can prevent premature ovarian failure (POF) by promoting autophagy and reducing granulosa cell apoptosis. This involves increasing estrogen receptor 1 (ESR1) and modulating the PI3K-AKT-mTOR pathway.

Area of Science:

  • Reproductive Biology
  • Cellular Biology
  • Endocrinology

Background:

  • Premature ovarian failure (POF) is linked to granulosa cell (GC) apoptosis.
  • Understanding mechanisms to prevent POF is crucial for reproductive health.

Purpose of the Study:

  • To investigate the preventative and therapeutic effects of melatonin (Mel) on POF.
  • To elucidate the cellular mechanisms underlying Mel's action in POF models.

Main Methods:

  • Utilized a POF mouse model treated with exogenous melatonin.
  • Performed intersecting target screening, Gene Ontology (GO), and KEGG pathway analysis.
  • Assessed GC autophagy markers (LC3/LC3-LL, Beclin1, p62), mitochondrial membrane potential, ATP content, and ESR1 expression.

Main Results:

  • Melatonin promoted estrogen secretion and improved ovarian function in POF mice.
  • Melatonin upregulated autophagy markers (LC3/LC3-LL, Beclin1) and increased mitochondrial potential and ATP in GCs.
  • Estrogen receptor 1 (ESR1) was identified as a key target, with Melatonin modulating the PI3K-AKT-mTOR pathway.

Conclusions:

  • Melatonin effectively mitigates POF by enhancing GC autophagy and reducing apoptosis.
  • Melatonin's mechanism involves upregulating ESR1 and inhibiting the PI3K-AKT-mTOR pathway, thereby protecting ovarian function.

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