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
Metadatos
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Franceschelli, Sara; Pesce, Mirko; Ferrone, Alessio; Gatta, Daniela Maria Pia; Patruno, Antonia; Lutiis, Maria Anna De; Quiles Morales, José Luis; Grilli, Alfredo; Felaco, Mario; Speranza, LorenzaEditorial
MDPI
Materia
Inflammation Nitric oxide Licochalcone C Adhesion molecule Cardiomyocytes Nuclear factor-κB Akt
Fecha
2017-03-23Referencia bibliográfica
Franceschelli, S.; et al. 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. International Journal of Molecular Sciences, 18(4): 690 (2017). [http://hdl.handle.net/10481/49125]
Patrocinador
The Italian Ministry for University and Research is acknowledged for financial support.Resumen
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.