Peperomins as anti-inflammatory agents that inhibit the NF-kappaB signaling pathway

The transcription factor nuclear factor kappaB (NF-kappaB) induces the expression of various inflammatory genes. In the common NF-kappaB signaling pathway, peperomin E and 2,6-didehydropeperomin B inhibited IkappaB degradation upon stimulation with TNF-alpha or interleukin-1. Consistent with these r...

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Veröffentlicht in:Bioorganic & medicinal chemistry letters 2009-08, Vol.19 (15), p.4084-4087
Hauptverfasser: Tsutsui, Chieko, Yamada, Yuriko, Ando, Masayoshi, Toyama, Daisuke, Wu, Jian-Lin, Wang, Liyan, Taketani, Shigeru, Kataoka, Takao
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container_end_page 4087
container_issue 15
container_start_page 4084
container_title Bioorganic & medicinal chemistry letters
container_volume 19
creator Tsutsui, Chieko
Yamada, Yuriko
Ando, Masayoshi
Toyama, Daisuke
Wu, Jian-Lin
Wang, Liyan
Taketani, Shigeru
Kataoka, Takao
description The transcription factor nuclear factor kappaB (NF-kappaB) induces the expression of various inflammatory genes. In the common NF-kappaB signaling pathway, peperomin E and 2,6-didehydropeperomin B inhibited IkappaB degradation upon stimulation with TNF-alpha or interleukin-1. Consistent with these results, peperomin E and 2,6-didehydropeperomin B blocked the TNF-alpha-induced activation of IkappaB kinase, while they had no direct effect on the IkappaB kinase activity. Our present results clearly demonstrate that peperomins inhibit the NF-kappaB signaling pathway by blocking IkappaB kinase activation.
doi_str_mv 10.1016/j.bmcl.2009.06.029
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subjects Anti-Inflammatory Agents - chemical synthesis
Anti-Inflammatory Agents - pharmacology
Benzodioxoles - chemical synthesis
Benzodioxoles - pharmacology
Cell Line, Tumor
Chemistry, Pharmaceutical - methods
Drug Design
Gene Expression Regulation
Humans
Inflammation - drug therapy
Interleukin-1 - metabolism
Models, Chemical
NF-kappa B - metabolism
Phosphorylation
Signal Transduction
Structure-Activity Relationship
Tumor Necrosis Factor-alpha - metabolism
title Peperomins as anti-inflammatory agents that inhibit the NF-kappaB signaling pathway
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