Suppression of cyclooxygenase-2 expression induced by Toll-like receptor 2 or 4 agonists by (E)-isopropyl 4-oxo-4-(2-oxopyrrolidin-1-yl)-2-butenoate
- Authors
- Lee, A-Neum; Park, Se-Jeong; Koh, Kwang Oh; Kim, Dae Young; Youn, Hyung-Sun
- Issue Date
- 31-Mar-2011
- Publisher
- 대한독성 유전단백체 학회
- Keywords
- Toll-like receptor; Lipopolysaccharide; Cyclooxygenase-2; Nuclear factor-kappa B; Fumaryl pyrrolidinone
- Citation
- Molecular & Cellular Toxicology, v.7, no.1, pp 39 - 44
- Pages
- 6
- Journal Title
- Molecular & Cellular Toxicology
- Volume
- 7
- Number
- 1
- Start Page
- 39
- End Page
- 44
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/16635
- DOI
- 10.1007/s13273-011-0006-0
- ISSN
- 1738-642X
2092-8467
- Abstract
- Inflammation can be initiated by invading microbial pathogens. Toll-like receptors (TLRs) recognize molecular structures derived from microbial pathogens and regulate the activation of innate immunity. TLR signaling pathways trigger the activation of nuclear factor-kappa B (NF-kappa B) transcription factor, leading to the induction of inflammatory gene products such as cyclooxygenase-2. Here, we present biochemical evidence that the fumaryl pyrroliclinone, (E)-isopropyl 4-oxo-4-(2-oxopyrrolidin-1-yl)-2-butenoate (IPOP), previously synthesized in our laboratory inhibits NF-kappa B activation induced by TLR agonists and overexpression of two downstream signaling components of TLRs. IPOP also inhibits TLR agonist-induced expression of cyclooxygenase-2. Our results suggest that IPOP can modulate TLR-mediated inflammatory responses and, potentially, the risk of many chronic inflammatory diseases.
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- Appears in
Collections - College of Medical Sciences > Department of Biomedical Laboratory Science > 1. Journal Articles
- College of Natural Sciences > Department of Chemistry > 1. Journal Articles
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