Curcumin Prevents Methylglyoxal-Induced Oxidative Stress and Apoptosis in Mouse Embryonic Stem Cells and Blastocysts

J Cell Physiol. 2005 Dec;205(3):379-86. doi: 10.1002/jcp.20408.

Abstract

Methylglyoxal (MG) is a reactive dicarbonyl compound endogenously produced mainly from glycolytic intermediates. Elevated MG levels in diabetes patients are believed to contribute to diabetic complications. MG is cytotoxic through induction of apoptosis. Curcumin, the yellow pigment of Curcuma longa, is known to have antioxidant and anti-inflammatory properties. In the present study, we examined the effect of curcumin on apoptotic biochemical events caused by incubation of ESC-B5 cells with MG. Curcumin inhibited the MG-induced DNA fragmentation, caspase-3 activation, cleavage of PARP, mitochondrial cytochrome c release, and JNK activation. Importantly, curcumin also inhibited the MG-stimulated increase of reactive oxygen species (ROS) in these cells. In addition, we demonstrated that curcumin prevented the MG-induced apoptosis of mouse blastocysts isolated from pregnant mice. Moreover, curcumin significantly reduced the MG-mediated impairment of blastocyst development from mouse morulas. The results support the hypothesis that curcumin inhibits MG-induced apoptosis in mouse ESC-B5 cells and blastocysts by blocking ROS formation and subsequent apoptotic biochemical events.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / administration & dosage
  • Antioxidants / pharmacology*
  • Apoptosis / drug effects*
  • Blastocyst / drug effects
  • Blastocyst / physiology
  • Caspase 3
  • Caspases / metabolism
  • Cell Death / drug effects
  • Cell Line
  • Curcumin / administration & dosage
  • Curcumin / pharmacology*
  • Cytochromes c / antagonists & inhibitors
  • Dose-Response Relationship, Drug
  • Embryo, Mammalian / cytology
  • Enzyme Activation / drug effects
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Mice
  • Mitochondria / metabolism
  • Oxidative Stress / drug effects*
  • Pyruvaldehyde / pharmacology*
  • Reactive Oxygen Species / antagonists & inhibitors
  • Reactive Oxygen Species / metabolism
  • Stem Cells / drug effects
  • Stem Cells / metabolism
  • Stem Cells / physiology*

Substances

  • Antioxidants
  • Reactive Oxygen Species
  • Pyruvaldehyde
  • Cytochromes c
  • JNK Mitogen-Activated Protein Kinases
  • Casp3 protein, mouse
  • Caspase 3
  • Caspases
  • Curcumin