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KMID : 1007520120210010279
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Food Science and Biotechnology
2012 Volume.21 No. 1 p.279 ~ p.283
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Luteolin Inhibits Inflammatory Responses by Downregulating the JNK, NF-κB, and AP-1 Pathways in TNF-α Activated HepG2 Cells
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Park Chung-Mu
Jin Kyong-Suk
Cho Chung-Won
Lee Yong-Woo
Huh Gyung-Hye
Cha Youn-Soo
Song Young-Sun
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Abstract
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The inhibitory mechanism of luteolin on tumor necrosis factor (TNF)-α-induced inflammation was investigated in HepG2 cells. Luteolin significantly suppressed TNF-α- 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)-κB and activator protein (AP)- 1, were also inhibited by luteolin treatment. Additionally, luteolin suppressed TNF-α-induced c-Jun N-terminal kinase (JNK) phosphorylation, which is crucially related to regulating inflammation. SP600125, a JNK selective inhibitor, abolished the TNF-α triggered inflammatory signaling cascade. These results suggest that luteolin attenuates inflammatory responses by blocking NF-κB and AP-1 activation through suppressed JNK phosphorylation in TNF-α-stimulated HepG2 cells.
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KEYWORD
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luteolin, inducible nitric oxide synthase (iNOS), nuclear factor (NF)-κB, activator protein-1 (AP- 1), c-Jun N-terminal kinase (JNK)
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