Action of Nrf2 and Keap1 in ARE-mediated NQO1 expression by quercetin

Tanigawa, Shunsuke; Fujii, Makoto; Hou, De‐Xing

doi:10.1016/j.freeradbiomed.2007.02.017

Cited by 431 publications

(331 citation statements)

References 46 publications

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“…Chlorogenic acid decreased ROS generation and stimulated the nuclear translocation of Nrf-2 and subsequently induced GSTA1 ARE-mediated GST activity in mice epithelial JB6 cells, providing a protective role against carcinogens [58]. Moreover, quercetin up-regulated mRNA Nrf2 expression and protein by inhibiting the ubiquitination and proteasomal turnover of Nrf2, and also repressed Kelch-like ECH-asso- ciating protein-1 (Keap1) which were essential for AREmediated NQO1 inhibition [64].…”

Section: Effects On Phase-i and -Ii Enzymesmentioning

confidence: 99%

Cancer chemoprevention and chemotherapy: Dietary polyphenols and signalling pathways

Ramos¹

2008

Molecular Nutrition Food Res

627

499

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Prevention of cancer through dietary intervention recently has received an increasing interest, and dietary polyphenols have become not only important potential chemopreventive, but also therapeutic, natural agents. Polyphenols have been reported to interfere at the initiation, promotion and progression of cancer. They might lead to the modulation of proteins in diverse pathways and require the integration of different signals for the final chemopreventive or therapeutic effect. Polyphenols have been demonstrated to act on multiple key elements in signal transduction pathways related to cellular proliferation, differentiation, apoptosis, inflammation, angiogenesis and metastasis; however, these molecular mechanisms of action are not completely characterized and many features remain to be elucidated. The aim of this review is to provide insights into the molecular basis of potential chemopreventive and therapeutic activities of dietary polyphenols with emphasis in their ability to control intracellular signalling cascades considered as relevant targets in a cancer preventive approach.

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Section: Effects On Phase-i and -Ii Enzymesmentioning

confidence: 99%

Cancer chemoprevention and chemotherapy: Dietary polyphenols and signalling pathways

Ramos¹

2008

Molecular Nutrition Food Res

627

499

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“…Qu has been found to activate cellular antioxidant system by increasing both transcriptional and post-transcriptional levels of Nrf-2, a transcription factor which induces expression of various antioxidants and Phase II detoxifying enzymes including NADPH quinone oxidoreductase 1, glutamate cysteine ligase, HO-1, and many others [78]. At the same time, Qu has been shown to reduce the level of Keap1 that keeps Nrf-2 in cytoplasm and thus blocks its activity through the modification of Keap1 protein rather than 26S proteasome degradation [79]. These mechanisms explain the depletion in serum HO-1 level on pre-treatment with Qu in GU bearing rats in the current study.…”

Section: Kotob Et Almentioning

confidence: 99%

Quercetin and Ellagic Acid in Gastric Ulcer Prevention: An Integrated Scheme of the Potential Mechanisms of Action From in Vivo Study

Kotob

Sayed

Mohamed

et al. 2018

Asian J Pharm Clin Res

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Objective: The present study was initiated to describe the gastroprotective role of quercetin (Qu) and ellagic acid (EA) on aspirin-induced gastric ulcer (GU) in rats.Methods: Forty adult female albino rats of Wistar strain were distributed into: Control group, GU group, Omeprazole group, Qu group, and EA group. Gross examination, biochemical analyses including serum adrenocorticotropic hormone (ACTH), serotonin (ST), ferritin, heme oxygenase-1 (HO-1), interleukin-2 (IL-2), advanced glycosylation end products (AGEs), and fibronectin (FN) levels were estimated. Moreover, histopathological and histochemical examinations of stomach tissue samples were carried out.Results: Gross examination of gastric mucosa of rats in GU group revealed hyperemia of the stomach mucosa. Furthermore, rats in GU group experienced a significant rise in serum ACTH, ferritin, HO-1, IL-2 and AGEs levels accompanied with significant drop in serum ST and FN levels versus control counterparts. Pre-treatment of GU group with Omeprazole, Qu or EA caused marked improvement in the measured biochemical parameters. Histopathological and histochemical examinations of stomach tissue samples documented the protective action of Omeprazole, Qu and EA with different degrees against GU caused by aspirin. Conclusion:As a conclusion to this study, we can state that both Qu and EA have gastroprotective effect against aspirin-induced GU in rat model. Of note, Qu showed superior impact than EA as an antiulcer agent in this study. The corresponding mechanisms are speculated to be associated with inhibiting stress-induced gastric lesion, attenuating the oxidative stress, iron chelation and blunting ferritin level, modulating inflammatory cascade, and promoting the healing process.

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“…Using ARE-luciferase reporter gene assays, quercetin has been shown to activate Nrf2 and upregulate NQO1. 125 Quercetin-mediated Nrf2 nuclear translocation through p38 and extracellular signal regulated kinase signaling and induction of cytoprotective genes protects human hepatocytes against ethanol-derived oxidative stress. 126 Exposure of NIH3T3 cells and human lung fibroblasts to quercetin induces the nuclear translocation of Nrf2, induces HO-1, and suppresses transforming growth factorbesimulated collagen synthesis.…”

Section: Nrf2 As a Therapeutic Targetmentioning

confidence: 99%

Nuclear Factor–Erythroid-2–Related Factor 2 in Aging and Lung Fibrosis

Swamy

Rajasekaran

Thannickal

2016

The American Journal of Pathology

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Aging and age-related diseases have been associated with elevated oxidative stress, which may be related to increased production of reactive species and/or a deficiency in antioxidant defenses. The nuclear factor-erythroid-2erelated factor 2 (Nrf2)-mediated antioxidant response pathway maintains cellular reduction-oxidation homeostasis by inducing the transcription of an array of cytoprotective genes. However, there is evidence of impaired Nrf2 response in aging contributing to age-related fibrotic diseases. Herein, we review mechanisms for the dysregulation of Nrf2 signaling in aging. This understanding will pave the way for the design of novel therapeutic strategies that restore Nrf2 signaling to reestablish cellular homeostasis in aging and age-related fibrotic diseases.

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Action of Nrf2 and Keap1 in ARE-mediated NQO1 expression by quercetin

Cited by 431 publications

References 46 publications

Cancer chemoprevention and chemotherapy: Dietary polyphenols and signalling pathways

Cancer chemoprevention and chemotherapy: Dietary polyphenols and signalling pathways

Quercetin and Ellagic Acid in Gastric Ulcer Prevention: An Integrated Scheme of the Potential Mechanisms of Action From in Vivo Study

Nuclear Factor–Erythroid-2–Related Factor 2 in Aging and Lung Fibrosis

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