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Comparison of (−)-Epigallocatechin-3-Gallate Elicited Liver and Small Intestine Gene Expression Profiles Between C57BL/6J Mice and C57BL/6J/Nrf2 (−/−) Mice

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Purpose

This study was conducted to study global gene expression profiles elicited by (−)-epigallocatechin-3-gallate (EGCG) in mouse liver and small intestine, as well as to identify EGCG-regulated Nrf2-dependent genes.

Methods

C57BL/6J and C57BL/6J/Nrf2(−/−) mice were given an oral dose of EGCG at 200 mg/kg or treated with vehicle. Both liver and small intestine were collected 3 h and 12 h after treatment. Total RNA was extracted from the tissues and gene expression profiles were analyzed using Affymetrix mouse genome 430 2.0 array and GeneSpring 6.1 software. Microarray data were validated using quantitative real-time reverse transcription-PCR chain reaction analysis.

Results

Genes that were either induced or suppressed more than two fold by EGCG treatment compared with vehicle treatment in the same genotype group were filtered using the GeneSpring software. Among these well-defined genes, 671 EGCG-regulated Nrf2-dependent genes and 256 EGCG-regulated Nrf2-independent genes were identified in liver, whereas 228 EGCG-regulated Nrf2-dependent genes and 98 EGCG-regulated Nrf2-independent genes were identified in the small intestine. Based on their biological functions, these genes mainly fall into the category of ubiquitination and proteolysis, electron transport, detoxification, transport, cell growth and apoptosis, cell adhesion, kinase and phosphatases, and transcription factors.

Conclusions

Genes expressed in mouse liver are more responsive to oral treatment of EGCG than those expressed in small intestine. EGCG could regulate many genes in both organs in an Nrf2-dependent manner. The identification of genes related to detoxification, transport, cell growth and apoptosis, cell adhesion, kinase, and transcription regulated by EGCG not only provide potential novel insight into the effect of EGCG on global gene expression and chemopreventive effects, but also point to the potential role of Nrf2 in these processes.

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Abbreviations

ABC:

ATP-binding cassette

ALOX:

arachidonate 12-lipoxygenase

ARE:

antioxidant response element

DNMT:

DNA methyltransferases

EGCG:

(−)-epigallocatechin-3-gallate

IGF-1R:

insulin-like growth factor 1 receptor gene

MAPK:

mitogen-activated protein kinase

MMP:

matrix metalloprotease

NF-κB:

nuclear factor kappa B

Nrf2:

nuclear factor E2-related factor 2

NOS:

nitric oxide synthase

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Acknowledgments

This work was supported in part by NIH Grants R01 CA094828 and R01-CA092515. We thank Mr. Curtis Krier at the Cancer Institute of New Jersey (CINJ) Core Expression Array Facility for assistance with the microarray analyses.

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Authors and Affiliations

  1. Graduate Program in Pharmaceutical Science, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey, 08854, USA

    Guoxiang Shen, Rong Hu, Sujit Nair, Wen Lin, Chung S. Yang & A.-N. Tony Kong

  2. Department of Pharmaceutics, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, 160 Frelinghuysen Road, Piscataway, New Jersey, 08854, USA

    Changjiang Xu, Mohit R. Jain & A.-N. Tony Kong

  3. Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey, 08854, USA

    Chung S. Yang

  4. Center for Cancer Prevention Research, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey, 08854, USA

    Chung S. Yang & A.-N. Tony Kong

  5. Department of Pathology, University of California, D440 Medical Sciences, Irvine, California, 92697, USA

    Jefferson Y. Chan

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  1. Guoxiang Shen
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  2. Changjiang Xu
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  3. Rong Hu
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  6. Wen Lin
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  9. A.-N. Tony Kong
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Correspondence to A.-N. Tony Kong.

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Guoxiang Shen and Changjiang Xu contributed equally to the present study.

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Shen, G., Xu, C., Hu, R. et al. Comparison of (−)-Epigallocatechin-3-Gallate Elicited Liver and Small Intestine Gene Expression Profiles Between C57BL/6J Mice and C57BL/6J/Nrf2 (−/−) Mice. Pharm Res 22, 1805–1820 (2005). https://doi.org/10.1007/s11095-005-7546-8

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  • DOI: https://doi.org/10.1007/s11095-005-7546-8

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