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. 2017 Aug 23;8:565. doi: 10.3389/fphar.2017.00565

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Copyright © 2017 Zhao, Pu, Zhao, Zhu, Li, Shen, Zhang, Zhang, Shen, Xiao and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Model of Teuvincenone F suppresses LPS-induced inflammatory cytokine production and NLRP3 inflammasome activation via attenuating K63-linked ubiquitination of NEMO. Upon LPS stimulated, TLR4 is activated, and then activates its downstream signaling pathways, promotes NEMO K63-linked ubiquitination, IKKα/β and NF-κB phosphorylation, following promotes LPS-induced inflammatory cytokine production and NLRP3 expression. Teuvincenone F suppresses LPS-induced K63-linked ubiquitination of NEMO and then inhibits IL-1β, IL-6, TNF-α, and NLRP3 mRNA expression, prevented inflammatory cytokines IL-6 and TNF-α production. Besides, decreasing NLRP3 expression affected NLRP3 inflammasome assemble and resulted in inhibiting NLRP3 inflammasome activation, following suppresses IL-1β/IL-18 maturation. In summary, Teuvincenone F suppresses LPS-induced inflammatory cytokines production via attenuating K63-linked ubiquitination of NEMO.