Protective effects of hydroxytyrosol on liver ischemia/reperfusion injury in mice

Mol Nutr Food Res. 2013 Jul;57(7):1218-27. doi: 10.1002/mnfr.201300010. Epub 2013 May 7.

Abstract

Scope: Hydroxytyrosol (HT), a main phenolic compound in olive oil, has been proved to be a potent antioxidant and has beneficial effects on health. However, the effect of HT on oxidative liver damage, as seen in ischemia/reperfusion (I/R) injury, is unknown. Here, we examined whether HT could protect liver against I/R injury.

Methods and results: By using a mouse model, we found that HT administration protects against hepatic I/R injury, as indicated by the decreased levels of serum aminotransferase and less parenchymal necrosis and apoptosis. Serum levels of tumor necrosis factor-α, interleukin-6, macrophage inflammatory protein 2, as well as reactive oxygen species (ROS) content in liver tissues, were all decreased by HT, the latter correlated with the reduction of hepatic malondialdehyde (an index of oxidative stress) content and increased activities and expressions of liver antioxidant enzymes superoxide dismutase and catalase. The protective effect was also seen in isolated hepatocytes anoxia/reoxygenation assay.

Conclusion: HT exerts protective effects against hepatic I/R injury in mice, which might be associated with its anti-oxidative, anti-inflammatory, and anti-apoptotic properties. HT may be an effective hepatoprotective agent and a promising candidate for the treatment of liver I/R injury.

Keywords: Hydroxytyrosol; Injury; Ischemia-reperfusion; Liver; Oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Apoptosis / drug effects
  • Catalase / metabolism
  • Cell Survival / drug effects
  • Chemokine CXCL2 / metabolism
  • Disease Models, Animal
  • Hepatocytes / drug effects
  • Hepatocytes / metabolism
  • In Situ Nick-End Labeling
  • Interleukin-6 / blood
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Oxidative Stress / drug effects
  • Phenylethyl Alcohol / analogs & derivatives*
  • Phenylethyl Alcohol / pharmacology
  • Reactive Oxygen Species / metabolism
  • Reperfusion Injury / drug therapy*
  • Superoxide Dismutase / metabolism
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Antioxidants
  • Chemokine CXCL2
  • Cxcl2 protein, mouse
  • Interleukin-6
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • 3,4-dihydroxyphenylethanol
  • Malondialdehyde
  • Catalase
  • Superoxide Dismutase
  • Phenylethyl Alcohol