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Cited by 107NF-κB Signaling PathwaysBioactive Compounds and Antitumor AgentsGenomics, phytochemicals, and oxidative stress

Inhibition of Nuclear Factor κB by Phenolic Antioxidants: Interplay between Antioxidant Signaling and Inflammatory Cytokine Expression

Ma, Qiang, Kinneer, Krista, Ye, Jianping, Chen, Bruce J·2003·Molecular Pharmacology
DOI 10.1124/mol.64.2.211
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Abstract

Phenolic antioxidants inhibit the induction of inflammatory cytokines by inflammatory stimuli. Here, we analyzed the mechanism by which the antioxidants inhibit LPS-induced expression of tumor necrosis factor alpha (TNFalpha) in macrophages. Hydroquinone and tert-butyl hydroquinone, prototypes of phenolic antioxidants, block lipopolysaccharide (LPS)-induced transcription of TNFalpha and a nuclear factor (NF)-kappaB-mediated reporter gene expression, suggesting NF-kappaB as a target in the inhibition. Analyses of the NF-kappaB activation pathway revealed that the antioxidants do not inhibit LPS-induced activation of the IkappaB kinase activity, degradation of IkappaBalpha, or translocation of activated NF-kappaB into the nucleus, but they do block the formation of NF-kappaB/DNA binding complexes. In vitro experiments showed that the antioxidants do not directly interfere with DNA binding of NF-kappaB. Structure-activity analyses suggest that inhibition of NF-kappaB function involves the redox cycling property of the antioxidants. These findings implicate a redox-sensitive factor important for the binding of NF-kappaB to its DNA recognition sequence as a target molecule in the inhibition of NF-kappaB function and inflammatory cytokine expression by phenolic antioxidants.

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  • The anti-inflammatory role of Nrf2 includes Nrf2-mediated inhibition of the pro-inflammatory NF-κB pathway and inhibition of expression of pro-inflammatory cytokines.

    “The anti-inflammatory role of Nrf2 also includes Nrf2-mediated inhibition of the pro-inflammatory NF-ΚB pathway and inhibition of expression of pro-inflammatory cytokines [195,196,197].”

    From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [195]

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Authors
Ma, Q., Kinneer, K., Ye, J., & Chen, B. J.
Affiliations
Centers for Disease Control and Prevention (US)
ORCID
Venue
Molecular Pharmacology
Publisher
Elsevier BV
Published
2003-08
Volume
64
Issue
2
Pages
211-219
ISSN
0026-895X (ISSN-L)
DOI
10.1124/mol.64.2.211
OpenAlex
W2018831724
Cited by
107
References
45
Citations by year
2025: 1 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 6 · 2019: 3 · 2018: 4 · 2017: 5 · 2016: 7 · 2015: 9 · 2014: 6 · 2013: 3 · 2012: 9
FWCI
1.24
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Molecular Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute for Occupational Safety and Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
Keywords
phenolic antioxidants, NF-κB inhibition, TNF-α, lipopolysaccharide, macrophages, inflammatory cytokines, hydroquinone, tert-butylhydroquinone, redox cycling, NF-kappaB DNA binding, IκB kinase, structure-activity relationship
MeSH terms
Animals, Antioxidants, Cells, Cultured, DNA, Macrophages, Oxidation-Reduction, Phenols, Transcription, Genetic, Tumor Necrosis Factor-alpha, Signal Transduction, Cytokines, NF-kappa B, Mice

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