Flavonoids inhibit iNOS production via mitogen activated proteins in lipoteichoic acid stimulated cardiomyoblasts.
Infective endocarditis is caused by oral commensal bacteria which are important etiologic agents in this disease and can induce release of nitric oxide (NO), promoting an inflammatory response in the endocardium. In this study, we investigated the properties of kaempherol, epigallocatechin, apigenin, and naringin in embryonic mouse heart cells (H9c2) treated with lipoteichoic acid (LTA) obtained from Streptococcus sanguinis. NO production was measured with the Griess method. Expression of inducible nitric oxide synthase (iNOS) was detected by reverse transcriptase polymerase chain reaction (RT-PCR). In addition, western blot assays and immunofluorescence staining were used to assess translocation of nuclear factor kappa beta (NF-κB), degradation of IκB, and activity of the mitogen activated protein (MAP) kinases extracellular signal-regulated kinase (ERK 1/2), p38, and c-Jun N-terminal kinase (JNK). And the effects of these flavonoids on cell viability were also assessed. Our results showed that flavonoids blocked activation of ERK, JNK, and p38 in cardiomyocytes treated with LTA. Moreover, the flavonoids showed no cytotoxic effects and blocked NF-κB translocation and IκB degradation and inhibited LTA-induced NF-κB promoter activity, iNOS expression and NO production. In conclusion these effects are consistent with some of the observed anti-inflammatory properties of other flavonoids.
Laboratorio de Bioquímica de la División de Estudios de Posgrado e Investigación, Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 México, D.F., Mexico. Electronic address: gloria@fo.odonto.unam.mx.
Gloria
G
Gutiérrez-Venegas
Laboratorio de Bioquímica de la División de Estudios de Posgrado e Investigación, Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 México, D.F., Mexico.
Jairo Agustín
JA
Ventura-Arroyo
Laboratorio de Bioquímica de la División de Estudios de Posgrado e Investigación, Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 México, D.F., Mexico.
Juan Antonio
JA
Arreguín-Cano
Laboratorio de Bioquímica de la División de Estudios de Posgrado e Investigación, Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 México, D.F., Mexico.
María Fernanda
MF
Ostoa-Pérez
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D005419:Flavonoids / Q000494:pharmacology*; D020672:I-kappa B Proteins / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D032386:Myoblasts, Cardiac / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors*; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D013298:Streptococcus sanguis / Q000378:metabolism; D013682:Teichoic Acids / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D005419:Flavonoids; D020672:I-kappa B Proteins; D008070:Lipopolysaccharides; D016328:NF-kappa B; D013682:Teichoic Acids; D009569:Nitric Oxide; C009900:lipoteichoic acid; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D020928:Mitogen-Activated Protein Kinases
Cardiomyoblasts; Flavonoids; Mitogen activated proteins; Nitric oxide