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Metformin prevented high glucose-induced endothelial reactive oxygen species via OGG1 in an AMPKα-Lin-28 dependent

Liangliang Tao1, Xiucai Fan1, Jin Sun1

  • 1Department of Cardiology, Jianhu Hospital Affiliated to Nantong University, China.

Life Sciences
|January 7, 2021
PubMed
Abstract

Insights

Metformin reduces high glucose-induced oxidative stress in endothelial cells by increasing 8-oxoguanine glycosylase (OGG1). This occurs via the AMPKα/Lin-28 pathway, improving vascular function in type 2 diabetes.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Vascular Biology

Background:

  • Obesity and type 2 diabetes are linked to vascular complications.
  • 8-Oxoguanine glycosylase (OGG1) plays a role in DNA repair and vascular disease.
  • The mechanism by which metformin affects endothelial oxidative stress via OGG1 is not fully understood.

Purpose of the Study:

  • To investigate if metformin suppresses endothelial reactive oxygen species (ROS) production through the OGG1 pathway.
  • To elucidate the molecular mechanisms linking metformin, OGG1, and endothelial ROS in high glucose conditions.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were treated with high glucose (HG) with or without metformin.
  • OGG1 and AMPKα levels were quantified.
  • HG-induced ROS production was measured using a DHE probe.

Main Results:

  • Metformin treatment upregulated OGG1, reducing HG-induced ROS in HUVECs.
  • OGG1 protein expression was linked to mRNA stability, influenced by AMPKα and Lin-28.
  • The OGG1-mediated reduction of ROS was partially dependent on the AHR/Nrf2 pathway.

Conclusions:

  • Metformin modulates HG-induced endothelial ROS via the AMPKα/Lin-28/OGG1 signaling pathway.
  • This pathway represents a potential therapeutic target for managing vascular complications in type 2 diabetes.
Keywords:
8-Oxoguanine glycosylaseLin-28MetforminReactive oxygen species

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