Targeting STAT1 by myricetin and delphinidin provides efficient protection of the heart from ischemia/reperfusion-induced injury

FEBS Lett. 2009 Feb 4;583(3):531-41. doi: 10.1016/j.febslet.2008.12.037. Epub 2008 Dec 29.

Abstract

Flavonoids exhibit a variety of beneficial effects in cardiovascular diseases. Although their therapeutic properties have been attributed mainly to their antioxidant action, they have additional protective mechanisms such as inhibition of signal transducer and activator of transcription 1 (STAT1) activation. Here, we have investigated the cardioprotective mechanisms of strong antioxidant flavonoids such as quercetin, myricetin and delphinidin. Although all of them protect the heart from ischemia/reperfusion-injury, myricetin and delphinidin exert a more pronounced protective action than quercetin by their capacity to inhibit STAT1 activation. Biochemical and computer modeling analysis indicated the direct interaction between STAT1 and flavonoids with anti-STAT1 activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anthocyanins / therapeutic use*
  • Antioxidants / therapeutic use
  • Cell Line, Tumor
  • Flavonoids / therapeutic use*
  • Humans
  • Male
  • Models, Molecular
  • Molecular Structure
  • Myocardial Reperfusion Injury / drug therapy*
  • Myocardial Reperfusion Injury / metabolism*
  • Myocardial Reperfusion Injury / pathology
  • Myocardial Reperfusion Injury / physiopathology
  • Rats
  • Rats, Sprague-Dawley
  • STAT1 Transcription Factor / metabolism*
  • Structure-Activity Relationship

Substances

  • Anthocyanins
  • Antioxidants
  • Flavonoids
  • STAT1 Transcription Factor
  • myricetin
  • delphinidin