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Int. J. Mol. Sci. 2017, 18(4), 690; doi:10.3390/ijms18040690

Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation

1
Department of Medicine and Science of Aging, University “G. D’Annunzio”, Chieti 66100, Italy
2
Department of Psychological, Health and Territorial Sciences, University “G. D’Annunzio”, Chieti 66100, Italy
3
Department of Physiology, Institute of Nutrition and Food Technology “José Mataix”, Biomedical Research Centre, University of Granada, Granada 18071, Spain
*
Author to whom correspondence should be addressed.
Academic Editor: Maurizio Battino
Received: 23 February 2017 / Revised: 9 March 2017 / Accepted: 20 March 2017 / Published: 23 March 2017
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Abstract

Polyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the effect of LicoC on the inflammatory response that characterizes septic myocardial dysfunction is poorly understood. The aim of this study was to determine whether LicoC exhibits anti-inflammatory properties on H9c2 cells that are stimulated with lipopolysaccharide. Our results have shown that LicoC treatment represses nuclear factor-κB (NF-κB) translocation and several downstream molecules, such as inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, LicoC has upregulated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signaling pathway. Finally, 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002), a specific PI3K inhibitor, blocked the protective effects of LicoC. These findings indicate that LicoC plays a pivotal role in cardiac dysfunction in sepsis-induced inflammation. View Full-Text
Keywords: inflammation; nitric oxide; licochalcone C; adhesion molecule; cardiomyocytes; nuclear factor-κB; Akt inflammation; nitric oxide; licochalcone C; adhesion molecule; cardiomyocytes; nuclear factor-κB; Akt
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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. (CC BY 4.0).

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Franceschelli, S.; Pesce, M.; Ferrone, A.; Gatta, D.M.P.; Patruno, A.; Lutiis, M.A.D.; Quiles, J.L.; Grilli, A.; Felaco, M.; Speranza, L. Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation. Int. J. Mol. Sci. 2017, 18, 690.

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