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Oxidative Medicine and Cellular LongevityVolume 2012 2012, Article ID 837104, 8 pages

Research ArticleDepartment of Biochemistry “G. Moruzzi”, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy

Received 10 February 2012; Accepted 22 March 2012

Academic Editor: Tullia Maraldi

Copyright © 2012 Cristina Angeloni and Silvana Hrelia. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Flavonoids possess several biological and pharmacological activities. Quercetin Q, a naturally occurring flavonoid, has been shown to downregulate inflammatory responses and provide cardioprotection. However, the mechanisms behind the anti-inflammatory properties of Q in cardiac cells are poorly understood. In inflammation, nitric oxide NO acts as a proinflammatory mediator and is synthesized by inducible nitric oxide synthase iNOS in response to pro-inflammatory agents such as lipopolysaccharide LPS, a causative agent in myocardial depression during sepsis. In the present study, we evaluated the protective effect of Q on rat cardiac dysfunction during sepsis induced by LPS. Pretreatment of H9c2 cardiomyoblasts with Q inhibited LPS-induced iNOS expression and NO production and counteracted oxidative stress caused by the unregulated NO production that leads to the generation of peroxynitrite and other reactive nitrogen species. In addition, Q pretreatment significantly counteracted apoptosis cell death as measured by immunoblotting of the cleaved caspase 3 and caspase 3 activity. Q also inhibited the LPS-induced phosphorylation of the stress-activated protein kinases JNK-SAPK and p38 MAP kinase that are involved in the inhibition of cell growth as well as the induction of apoptosis. In conclusion, these results suggest that Q might serve as a valuable protective agent in cardiovascular inflammatory diseases.

Author: Cristina Angeloni and Silvana Hrelia

Source: https://www.hindawi.com/


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