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Targeting Cell Signaling and Apoptotic Pathways by Luteolin: Cardioprotective Role in Rat Cardiomyocytes Following Ischemia/Reperfusion

by Tongda Xu 1,2, Dongye Li 1,2,* and Dehua Jiang 2
1
The First Clinical College, Nanjing Traditional Chinese Medicine University, Nanjing, Jiangsu 210046, China
2
Research Institute of Cardiovascular Diseases, Xuzhou Medical College, Xuzhou, Jiangsu 221002, China
*
Author to whom correspondence should be addressed.
Nutrients 2012, 4(12), 2008-2019; https://doi.org/10.3390/nu4122008
Received: 31 October 2012 / Revised: 28 November 2012 / Accepted: 5 December 2012 / Published: 12 December 2012
(This article belongs to the Special Issue Polyphenols and Human Health)
Myocardial ischemia often results in damaged heart structure and function, which can be restored through ischemia/reperfusion (I/R) in most cases. However, I/R can exacerbate myocardial ischemia reperfusion injury (IRI). Luteolin, a widely distributed flavonoid, a member of a group of naturally occurring polyphenolic compounds found in many fruits, vegetables and medicinal herbs, has been reported to exhibit anti-inflammatory, antioxidant and anti-carcinogenic activities. In recent years, luteolin has been shown to play an important role in the cardioprotection of IRI. However, its role and mechanism in cardioprotection against IRI has not been clearly elucidated with respect to the apoptosis pathway. The purpose of this paper is to review luteolin’s anti-apoptotic role and mechanism following I/R in rats, and indicate luteolin as a potential candidate for preventing and treating cardiovascular diseases. View Full-Text
Keywords: luteolin; ischemia/reperfusion (I/R); ischemia reperfusion injury (IRI); cardiomyocytes; mechanism; apoptosis luteolin; ischemia/reperfusion (I/R); ischemia reperfusion injury (IRI); cardiomyocytes; mechanism; apoptosis
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Xu, T.; Li, D.; Jiang, D. Targeting Cell Signaling and Apoptotic Pathways by Luteolin: Cardioprotective Role in Rat Cardiomyocytes Following Ischemia/Reperfusion. Nutrients 2012, 4, 2008-2019.

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