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Targeting STAT1 by myricetin and delphinidin provides efficient protection of the heart from ischemia/reperfusion‐induced injury
Author(s) -
Scarabelli Tiziano M.,
Mariotto Sofia,
Abdel-Azeim Safwat,
Shoji Kazuo,
Darra Elena,
Stephanou Anastasis,
Chen-Scarabelli Carol,
Marechal Jean Didier,
Knight Richard,
Ciampa Anna,
Saravolatz Louis,
de Prati Alessandra Carcereri,
Yuan Zhaokan,
Cavalieri Elisabetta,
Menegazzi Marta,
Latchman David,
Pizza Cosimo,
Perahia David,
Suzuki Hisanori
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.12.037
Subject(s) - myricetin , delphinidin , quercetin , pharmacology , chemistry , stat1 , antioxidant , reperfusion injury , ischemia , luteolin , biochemistry , medicine , kaempferol , signal transduction , cyanidin
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.