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

• Published in: International journal of molecular sciences 2017-03, Vol.18 (4), p.690
• Main Authors: Franceschelli, Sara, Pesce, Mirko, Ferrone, Alessio, Gatta, Daniela Maria Pia, Patruno, Antonia, Lutiis, Maria Anna De, Quiles, José Luis, Grilli, Alfredo, Felaco, Mario, Speranza, Lorenza
• Format: Article
• Language: English
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Animals; Anti-inflammatory agents; Anti-Inflammatory Agents - pharmacology; Antioxidants; Apoptosis; Biological effects; Biological properties; Cardiomyocytes; Cell adhesion; Cell adhesion & migration; Cell adhesion molecules; Cell Line; Chalcones - pharmacology; Cytotoxicity; Flavonoids; Gene expression; Inflammation; Inflammatory response; Intercellular adhesion molecule 1; Intercellular Adhesion Molecule-1 - metabolism; Kinases; Lipopolysaccharides; Lipopolysaccharides - toxicity; NF-kappa B - metabolism; NF-κB protein; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - metabolism; Nitric Oxide Synthase Type III - metabolism; Nitric-oxide synthase; Phosphatidylinositol 3-Kinases - antagonists & inhibitors; Phosphatidylinositol 3-Kinases - metabolism; Polyphenols; Proteins; Proto-Oncogene Proteins c-akt - metabolism; Rats; Sepsis; Signal transduction; Signal Transduction - drug effects; Vascular cell adhesion molecule 1
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms18040690

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 , 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(4 )-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.