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Arch Pharm Res. 2017 Feb;40(2):240-249. doi: 10.1007/s12272-016-0756-2. Epub 2016 May 18.

Apigenin reduce lipoteichoic acid-induced inflammatory response in rat cardiomyoblast cells.

Author information

1
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.
2
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.

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.

KEYWORDS:

Apigenin; Cardiomyocytes; Cyclooxygenase-2; Flavonoid; Lipoteichoic acid; Mitogen activated protein kinases

PMID:
27193174
DOI:
10.1007/s12272-016-0756-2
[Indexed for MEDLINE]

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