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Zinc inhibits high glucose-induced apoptosis in peritoneal mesothelial cells

Xiuli Zhang1, Dan Liang, Baolei Guo

  • 1Department of Nephrology, The First Affiliated Hospital of China Medical University, 155th Nanjing North Street, Shenyang, Liaoning, 110001, People's Republic of China.

Biological Trace Element Research
|July 25, 2012
PubMed

Insights

Zinc supplementation protects rat peritoneal mesothelial cells from high glucose-induced apoptosis. This essential mineral reduces oxidative stress and key apoptotic markers, promoting cell survival.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Toxicology

Background:

  • Apoptosis, or programmed cell death, is crucial for tissue homeostasis.
  • Zinc (Zn) influences apoptosis, but its role in peritoneal mesothelial cells (PMCs) is unclear.
  • High glucose (HG) can induce apoptosis in PMCs, a process relevant to peritoneal dialysis complications.

Purpose of the Study:

  • To investigate the protective effects of zinc supplementation against high glucose-induced apoptosis in rat peritoneal mesothelial cells (RPMCs).
  • To elucidate the molecular mechanisms underlying zinc's action in RPMCs under high glucose conditions.

Main Methods:

  • Rat peritoneal mesothelial cells (RPMCs) were treated with high glucose (HG) with or without zinc (Zn) supplementation.
  • Assessed apoptosis markers including reactive oxygen species (ROS) production, Fas receptor/ligand (FasR/FasL) expression, and caspase activation (caspase-8, caspase-3).
  • Mitochondrial cytochrome c release and activation of survival pathways (PI3K/Akt, MAPK/ERK) were analyzed.

Main Results:

  • Zinc supplementation significantly inhibited HG-induced apoptosis in RPMCs.
  • Zn attenuated ROS production, suppressed sFasR and sFasL overexpression, and reduced caspase-8 and caspase-3 activation.
  • Zn prevented cytochrome c release from mitochondria and activated the PI3K/Akt and MAPK/ERK survival pathways.

Conclusions:

  • Zinc exerts protective effects against high glucose-induced apoptosis in rat peritoneal mesothelial cells.
  • Mechanisms include indirect antioxidant effects, inhibition of caspase activation, and promotion of cell survival pathways.
  • Zinc may be a potential therapeutic agent to mitigate high glucose-induced cellular damage in PMCs.

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