title: Apigenin reduce lipoteichoic acid-induced inflammatory response in rat cardiomyoblast cells.
abstract: Infective endocarditis is caused by Streptococcus sanguinis present in dental plaque, which can induce inflammatory responses in the endocardium. The present study depicts research on the properties of apigenin in embryonic mouse heart cells (H9c2) treated with lipoteichoic acid (LTA) obtained from S. sanguinis. Interleukin-1β and cyclooxygenase (COX)-2 expression were detected by reverse transcriptase polymerase chain reaction. In addition, western blot assays and immuno-fluorescence staining were used to assess translocation of nuclear factor kappa beta (NF-κB), degradation of IκB, as well as activity of the mitogen activated protein kinases: extracellular signal-regulated kinase (ERK)1/2, p38, and c-Jun N-terminal kinase (JNK). Effect of apigenin on cell viability was equally assessed in other experimental series. Our results showed that apigenin blocked activation of ERK, JNK, and p38 in cardiomyocytes treated with LTA in a dose-dependent fashion. Moreover, apigenin showed no cytotoxic effects; it blocked NF-κB translocation and IκB degradation. Our findings suggested that apigenin possessed potential value in the treatment of infectious endocarditis.
authors.affiliation: Laboratorio de Bioquímica de la División de Estudios de Posgrado e Investigación de la Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510, Ciudad de México, DF, Mexico. gloria@fo.odonto.unam.mx.
authors.forename: Gloria
authors.initials: G
authors.lastname: Gutiérrez-Venegas
authors.affiliation: Laboratorio de Bioquímica de la División de Estudios de Posgrado e Investigación de la Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510, Ciudad de México, DF, Mexico.
authors.forename: Zeltzin
authors.initials: Z
authors.lastname: González-Rosas
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D047310:Apigenin / Q000494:pharmacology* / Q000627:therapeutic use; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004697:Endocarditis, Bacterial / Q000188:drug therapy* / Q000382:microbiology; D051550:I-kappa B Kinase / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases; D008070:Lipopolysaccharides / Q000276:immunology; D051379:Mice; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D032386:Myoblasts, Cardiac / Q000187:drug effects* / Q000276:immunology; D016328:NF-kappa B / Q000378:metabolism; D051381:Rats; D015398:Signal Transduction; D013298:Streptococcus sanguis / Q000276:immunology*; D013682:Teichoic Acids / Q000276:immunology; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D013682:Teichoic Acids; C009900:lipoteichoic acid; D047310:Apigenin; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D051550:I-kappa B Kinase; D048031:JNK Mitogen-Activated Protein Kinases; C535148:Mapk1 protein, mouse; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases
keywords: Apigenin; Cardiomyocytes; Cyclooxygenase-2; Flavonoid; Lipoteichoic acid; Mitogen activated protein kinases