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Melatonin inhibits autophagy in TM3 cells via AKT/FOXO1 pathway

Zhiqiang Li1,2, Hongtao Wang1,2, Kaiyan Zhang1,2

  • 1Joint Laboratory of the Modern Agricultural Technology International Cooperation, Ministry of Education, Jilin Agricultural University, 130118, Changchun, Jilin, China.

Molecular Biology Reports
|January 8, 2022
PubMed
Abstract

Insights

Melatonin inhibits autophagy in mouse Leydig cells by regulating the AKT/FOXO1 pathway. This study clarifies the mechanism by which melatonin affects autophagy and oxidative stress.

Area of Science:

  • Reproductive Biology
  • Cellular Biology
  • Endocrinology

Background:

  • Melatonin's role in regulating mouse Leydig cell apoptosis and autophagy is known, but the precise mechanism remains elusive.
  • Understanding melatonin's molecular targets is crucial for its therapeutic applications in reproductive health.

Purpose of the Study:

  • To elucidate the specific mechanism by which melatonin regulates autophagy in mouse Leydig cells.
  • To investigate the involvement of the AKT/FOXO1 pathway in melatonin-mediated autophagy inhibition.

Main Methods:

  • Utilized the TM3 cell line and hydrogen peroxide (H2O2) to induce autophagy.
  • Assessed autophagy-related gene and protein expression using qRT-PCR and Western blot.
  • Measured cellular reactive oxygen species (ROS) levels via flow cytometry.

Main Results:

  • Melatonin significantly inhibited autophagy, decreasing Becn1, LC3, and FOXO1 expression while increasing p62 and pAKT expression.
  • Melatonin treatment led to a significant reduction in cellular ROS levels.
  • Inhibition of AKT reversed melatonin's autophagy-suppressing effects, and FOXO1 knockdown did not alter autophagy or ROS levels.

Conclusions:

  • Melatonin inhibits H2O2-induced autophagy in TM3 cells via the AKT/FOXO1 signaling pathway.
  • The findings highlight the AKT/FOXO1 pathway as a key mediator of melatonin's effects on autophagy and oxidative stress in Leydig cells.
Keywords:
AKTAutophagyFOXO1MelatoninMouseTM3 cells

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