Dihydromyricetin suppresses TNF-[alpha]-induced NF-[kappa]B activation and target gene expression

Nuclear factor-kappa B (NF-[kappa]B) has been reported to play a pivotal role in many physiological processes including inflammation, apoptosis, and angiogenesis. We discovered a potent natural NF-[kappa]B inhibitor, dihydromyricetin, from the traditional herb Ampelopsis grossedentata, which has a l...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2016-11, Vol.422 (1-2), p.11
Main Authors: Tang, Nina, Ma, Juan, Wang, Ke Si, Mi, Chunliu, Lv, Ying, Piao, Lian Xun, Xu, Guang Hua, Li, Xuezheng, Lee, Jung Joon, Jin, Xuejun
Format: Article
Language:English
Subjects:
Anatomy & physiology
Apoptosis
B cells
Gene expression
Genes
Inflammatory diseases
Nuclear medicine
Translocation
Tumor necrosis factor
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Summary:Nuclear factor-kappa B (NF-[kappa]B) has been reported to play a pivotal role in many physiological processes including inflammation, apoptosis, and angiogenesis. We discovered a potent natural NF-[kappa]B inhibitor, dihydromyricetin, from the traditional herb Ampelopsis grossedentata, which has a long history of use in food and medicine. In this study, we demonstrated the effect of dihydromyricetin on NF-[kappa]B activation in TNF-[alpha]-induced HeLa cells. Dihydromyricetin was found to markedly inhibit the phosphorylation and degradation of the inhibitor of NF-[kappa]B alpha (I[kappa]B[alpha]), and subsequent nuclear translocation of p65. Dihydromyricetin also has an impact on upstream signaling of IKK through the inhibition of expression of adaptor proteins, TNF receptor-associated factor 2 (TRAF2), and receptor-interacting protein 1 (RIP1). Furthermore, the current results reveal that dihydromyricetin led to the downregulation of target genes involved in inflammation, proliferation, as well as potentiation of TNF-[alpha]-induced apoptosis through suppressing the activation of NF-[kappa]B. In conclusion, our data indicate that dihydromyricetin may be a potentially useful therapeutic agent for inflammatory diseases.
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-016-2799-6