Chung Mu Park, Kyong-Suk Jin, Chung Won Cho, Yong-Woo Lee, Gyung-Hye Huh, Youn-Soo Cha, Young Sun Song
Abstract:
The inhibitory mechanism of luteolin on tumor necrosis factor (TNF)-a-induced inflammation was investigated in HepG2 cells. Luteolin significantly suppressed TNF-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)-?B and activator protein (AP)-1, were also inhibited by luteolin treatment. Additionally, luteolin suppressed TNF-a-induced c-Jun N-terminal kinase (JNK) phosphorylation, which is crucially related to regulating inflammation. SP600125, a JNK selective inhibitor, abolished the TNF-a triggered inflammatory signaling cascade. These results suggest that luteolin attenuates inflammatory responses by blocking NF-?B and AP-1 activation through suppressed JNK phosphorylation in TNF-a-stimulated HepG2 cells.
Sources: Click HERE
Keywords:
luteolin, inducible nitric oxide synthase (iNOS), nuclear factor (NF)-?B, activator protein-1 (AP-1), c-Jun N-terminal kinase (JNK)
