Luteolin inhibits inflammatory responses by downregulating the JNK, NF- Delta kB, and AP-1 pathways in TNF- Delta a activated HepG2 cells

The inhibitory mechanism of luteolin on tumor necrosis factor (TNF)- Delta *a-induced inflammation was investigated in HepG2 cells. Luteolin significantly suppressed TNF- Delta *a-stimulated inducible nitric oxide synthase (iNOS) expression in a dose-dependent manner without cytotoxicity. Phosphoryl...

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Bibliographic Details
Published in:Food science and biotechnology 2012-02, Vol.21 (1), p.279-283
Main Authors: Park, Chung Mu, Jin, Kyong-Suk, Cho, Chung Won, Lee, Yong-Woo, Huh, Gyung-Hye, Cha, Youn-Soo, Song, Young Sun
Format: Article
Language:English
Subjects:
Activator protein 1
c-Jun amino-terminal kinase
Cytotoxicity
Inflammation
Nitric-oxide synthase
Nuclear transport
Phosphorylation
Signal transduction
Transcription factors
Tumor necrosis factor
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Summary:The inhibitory mechanism of luteolin on tumor necrosis factor (TNF)- Delta *a-induced inflammation was investigated in HepG2 cells. Luteolin significantly suppressed TNF- Delta *a-stimulated inducible nitric oxide synthase (iNOS) expression in a dose-dependent manner without cytotoxicity. Phosphorylation and nuclear translocation of both transcription factors, nuclear factor (NF)- Delta *kB and activator protein (AP)-1, were also inhibited by luteolin treatment. Additionally, luteolin suppressed TNF- Delta *a-induced c-Jun N-terminal kinase (JNK) phosphorylation, which is crucially related to regulating inflammation. SP600125, a JNK selective inhibitor, abolished the TNF- Delta *a triggered inflammatory signaling cascade. These results suggest that luteolin attenuates inflammatory responses by blocking NF- Delta *kB and AP-1 activation through suppressed JNK phosphorylation in TNF- Delta *a-stimulated HepG2 cells.
ISSN:1226-7708
DOI:10.1007/s10068-012-0037-x