Cited by 739Genomics, phytochemicals, and oxidative stressNF-κB Signaling PathwaysRedox biology and oxidative stress

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Activation of Nrf2-antioxidant signaling attenuates NFκB-inflammatory response and elicits apoptosis

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Li, Wenge, Khor, Tin Oo, Xu, Changjiang, Shen, Guoxiang, Jeong, Woo-Sik, Yu, Siwang, Kong, Ah-Ng·2008·Biochemical Pharmacology

DOI 10.1016/j.bcp.2008.07.017PMC PMC2610259

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Abstract

Oxidative stress has been implicated in the etiology of neurodegenerative disease, cancer and aging. Indeed, accumulation of reactive oxygen and nitrogen species generated by inflammatory cells that created oxidative stress is thought to be one of the major factor by which chronic inflammation contributes to neoplastic transformation as well as many other diseases. We have recently reported that mice lacking nuclear factor-erythroid 2-related factor 2 (Nrf2) are more susceptible to dextran sulfate sodium (DSS)-induced colitis and colorectal carcinogenesis. Nrf2 is a basic leucine zipper redox-sensitive transcriptional factor that plays a center role in ARE (antioxidant response element)-mediated induction of phase II detoxifying and antioxidant enzymes. We found that increased susceptibility of Nrf2 deficient mice to DSS-induced colitis and colorectal cancer was associated with decreased expression of antioxidant/phase II detoxifying enzymes in parallel with upregulation of pro-inflammatory cytokines/biomarkers. These findings suggest that Nrf2 may play an important role in defense against oxidative stress possibly by activation of cellular antioxidant machinery as well as suppression of pro-inflammatory signaling pathways. In addition, in vivo and in vitro data generated from our laboratory suggest that many dietary compounds can differentially regulate Nrf2-mediated antioxidant/anti-inflammatory signaling pathways as the first line defense or induce apoptosis once the cells have been damaged. In this review, we will summarize our thoughts on the potential cross-talks between Nrf2 and NFkappaB pathways. Although the mechanisms involved in the cross-talk between these signaling pathways are still illusive, targeting Nrf2-antioxidative stress signaling is an ideal strategy to prevent or treat oxidative stress-related diseases.

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Oxidative stress sensor Keap1 functions as an adaptor for Cul3-based E3 ligase to regulate proteasomal degradation of Nrf2
Kobayashi, A., Kang, M.-I., Okawa, H., Ohtsuji, M., Zenke, Y., Chiba, T., Igarashi, K., & Yamamoto, M. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.24.16.7130-7139.2004 · Cited by 2,224
Nrf2–Keap1 defines a physiologically important stress response mechanism
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“enhancer called antioxidant response element (ARE), and eventually recruits the whole transcription machinery including the RNA polymerase II to transcribe phase II/III genes [1].”
Background
Keap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex
Zhang, D. D., Lo, S., Cross, J. V., Templeton, D. J., & Hannink, M. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.24.24.10941-10953.2004 · Cited by 1,284
The Keap1-BTB Protein Is an Adaptor That Bridges Nrf2 to a Cul3-Based E3 Ligase: Oxidative Stress Sensing by a Cul3-Keap1 Ligase
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Oxidative and Electrophilic Stresses Activate Nrf2 through Inhibition of Ubiquitination Activity of Keap1
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BTB Protein Keap1 Targets Antioxidant Transcription Factor Nrf2 for Ubiquitination by the Cullin 3-Roc1 Ligase
Furukawa, M., & Xiong, Y. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.25.1.162-171.2005 · Cited by 759
Keap1 Recruits Neh2 through Binding to ETGE and DLG Motifs: Characterization of the Two-Site Molecular Recognition Model
Tong, K. I., Katoh, Y., Kusunoki, H., Itoh, K., Tanaka, T., & Yamamoto, M. (2006) · Molecular and Cellular Biology · doi:10.1128/mcb.26.8.2887-2900.2006 · Cited by 759 · cited 2×
“, a high affinity phase I binding, mediated by the ETGE motif and a low affinity phase II binding mediated by the DLG motif, has been distinguished [8].”
Background
Structural basis for defects of Keap1 activity provoked by its point mutations in lung cancer
Padmanabhan, B., Tong, K. I., Ohta, T., Nakamura, Y., Scharlock, M., Ohtsuji, M., Kang, M.-I., Kobayashi, A., Yokoyama, S., & Yamamoto, M. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.01.013 · Cited by 735 · cited 3×
“The geometric distance between the two Kelch domains matches perfectly with the length of this alpha helix [10].”
BackgroundInfluential
NF-κB/p65 antagonizes Nrf2-ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK
Liu, G.-H., Qu, J., & Shen, X. (2008) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2008.01.002 · Cited by 697 · cited 3×
“[21] Liu GH, Qu J, Shen X. NF-kappaB/p65 antagonizes Nrf2-ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK.”
BackgroundInfluential
Nrf2-Deficient Mice Have an Increased Susceptibility to Dextran Sulfate Sodium–Induced Colitis
Khor, T. O., Huang, M., Kwon, K. H., Chan, J. Y., Reddy, B. S., & Kong, A. T. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-3562 · Cited by 530
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Authors: Li, W., Khor, T. O., Xu, C., Shen, G., Jeong, W.-S., Yu, S., & Kong, A.-N.
Affiliations: Rutgers, The State University of New Jersey (US)
Corresponding author: Kong, Ah-Ng
ORCID: Li, Wenge
Shen, Guoxiang
Jeong, Woo-Sik
Yu, Siwang
Kong, Ah-Ng
Venue: Biochemical Pharmacology
Publisher: Elsevier BV
Published: 2008-12
Volume: 76
Issue: 11
Pages: 1485-1489
ISSN: 0006-2952 (ISSN-L)
DOI: 10.1016/j.bcp.2008.07.017
PMC: PMC2610259
OpenAlex: W2064452102
Cited by: 738
References: 25
Citations by year: 2026: 17 · 2025: 32 · 2024: 28 · 2023: 43 · 2022: 66 · 2021: 59 · 2020: 52 · 2019: 58 · 2018: 58 · 2017: 43 · 2016: 52 · 2015: 52 · 2014: 29 · 2013: 48 · 2012: 33
FWCI: 9.32
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Biochemical Pharmacology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (R01CA118947, CA094828, R01CA073674, CA-118947, CA073674, R01CA094828)
National Institute of Environmental Health Sciences (P30ES005022)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: Nrf2, NF-κB, oxidative stress, antioxidant response element, phase II enzymes, colitis, colorectal cancer, inflammatory cytokines, apoptosis, dietary compounds, chronic inflammation, neurodegenerative diseases, aging
MeSH terms: Animals, Antioxidants, Signal Transduction, NF-kappa B, Apoptosis, Oxidative Stress, Inflammation Mediators, NF-E2-Related Factor 2, Mice

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Activation of Nrf2-antioxidant signaling attenuates NFκB-inflammatory response and elicits apoptosis

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