Hypoxia-reoxygenation differentially stimulates stress-activated protein kinases in primary-cultured rat hepatocytes

Transpl Int. 2000:13 Suppl 1:S597-9. doi: 10.1007/s001470050410.

Abstract

Organ injury after ischemia and reperfusion (I/R) remains one of the most important limiting factors in liver surgery and transplantation. Oxygen-free radical (OFR) generation is considered a major cause of this damage. JNK1/SAPK1, a member of MAPK family, regulates cell adaptation to stressful conditions. The aim of this study was to determine if hypoxia-reoxygenation (H/R) can activate JNK1/SAPK1 and if OFR are involved in this activation. Primary cultured rat hepatocytes isolated from other liver cells and blood flow were submitted to warm and cold H/R phases mimicking surgical and transplant conditions. JNK1/SAPK1 was activated by both warm and cold H/R. Deferoxamine (1 mM), di-phenyleneiodonium (50 microM) and N-acetylcysteine (10 mM) significantly inhibited this kinase activation.

MeSH terms

  • Animals
  • Cell Hypoxia / physiology*
  • Cells, Cultured
  • Enzyme Activation
  • Hepatocytes / cytology
  • Hepatocytes / enzymology
  • Hepatocytes / physiology*
  • Male
  • Mitogen-Activated Protein Kinase 8
  • Mitogen-Activated Protein Kinases / metabolism*
  • Oxidative Stress / physiology*
  • Rats
  • Rats, Wistar
  • Temperature

Substances

  • Mitogen-Activated Protein Kinase 8
  • Mitogen-Activated Protein Kinases