Isobavachalcone suppresses the TRIF-dependent signaling pathway of Toll-like receptors
- Authors
- Shin, Seokwon; Park, Jayeon; Lee, Ye Eun; Ko, Hanbin; Youn, Hyung-Sun
- Issue Date
- Mar-2022
- Publisher
- John Wiley & Sons Ltd.
- Keywords
- inflammation; isobavachalcone; nuclear factor-kappa B; Toll-like receptors; TRIF
- Citation
- Archiv der Pharmazie, v.355, no.3, pp 8 - 9
- Pages
- 2
- Journal Title
- Archiv der Pharmazie
- Volume
- 355
- Number
- 3
- Start Page
- 8
- End Page
- 9
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/20524
- DOI
- 10.1002/ardp.202100404
- ISSN
- 0365-6233
1521-4184
- Abstract
- Toll-like receptors (TLRs) are integral membrane-bound receptors that are central to innate and adaptive immune responses. They are known to activate a cascade of downstream signals to induce the secretion of inflammatory cytokines, chemokines, and type I interferons. Dysregulated activation of TLR signaling pathways can induce the activation of various transcription factors, such as nuclear factor kappa B (NF-kappa B) and interferon regulatory factor 3 (IRF3). TLRs act via MyD88- and TRIF-mediated pathways to induce inflammatory responses. To evaluate the therapeutic potential of isobavachalcone (IBC), a natural chalcone component of Angelica keiskei, we examined its effects on signal transduction via TLR signaling pathways. IBC inhibited the activation of NF-kappa B and IRF3 induced by TLR agonists and their target genes. IBC also inhibited the activation of NF-kappa B and IRF3 induced by overexpression of downstream signaling components of TLR signaling pathways. These results suggest that IBC can regulate both MyD88- and TRIF-dependent signaling pathways of TLRs, resulting in a dramatic increase of new therapeutic options for various inflammatory diseases involving TLRs.
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Collections - College of Medical Sciences > Department of Biomedical Laboratory Science > 1. Journal Articles
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