Research Article

Effects of the black tea polyphenol theaflavin-2 on apoptotic and inflammatory pathways in vitro and in vivo

  1. Alexander Gosslau1,2,*,
  2. David Li En Jao2,
  3. Mou-Tuan Huang3,
  4. Chi-Tan Ho4,
  5. Dave Evans1,†,
  6. Nancy E. Rawson1,
  7. Kuang Yu Chen2,3

Article first published online: 28 JUL 2010

DOI: 10.1002/mnfr.201000165

Issue

Molecular Nutrition & Food Research

Molecular Nutrition & Food Research

Volume 55, Issue 2, pages 198–208, February 2011

Additional Information

How to Cite

Gosslau, A., En Jao, D. L., Huang, M.-T., Ho, C.-T., Evans, D., Rawson, N. E. and Chen, K. Y. (2011), Effects of the black tea polyphenol theaflavin-2 on apoptotic and inflammatory pathways in vitro and in vivo. Mol. Nutr. Food Res., 55: 198–208. doi: 10.1002/mnfr.201000165

Author Information

  1. 1

    WellGen Inc., Commercialization Center for Innovative Technologies, North Brunswick, NJ, USA

  2. 2

    Department of Chemistry and Chemical Biology, Rutgers, Piscataway, NJ, USA

  3. 3

    Susan Lehman Cullman Laboratory for Cancer Research, Rutgers, Piscataway, NJ, USA

  4. 4

    Department of Food Science and Center for Advanced Food Technologies, Rutgers, North Brunswick, NJ, USA

  1. †

    deceased

*Department of Chemistry and Chemical Biology, Rutgers University, 610 Taylor Road, Piscataway, NJ 08854-8087, USA Fax: +1-732-445-5312

  1. †

    deceased

Publication History

  1. Issue published online: 3 FEB 2011
  2. Article first published online: 28 JUL 2010
  3. Manuscript Accepted: 19 JUN 2010
  4. Manuscript Revised: 28 MAY 2010
  5. Manuscript Received: 7 APR 2010

Funded by

  • Commission on Science and Technology, State of New Jersey as a component of the Pioneering Nutraceutical Research Program
  • NIH-NCCAM Grant. Grant Number: 1R43AT001143-01A1

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Keywords:

  • Apoptosis;
  • Cyclooxygenase-2;
  • Inflammation;
  • Mitochondria;
  • Theaflavin

Abstract

Scope: Theaflavin-2 (TF-2), a major component of black tea extract, induces apoptosis of human colon cancer cells and suppresses serum-induced cyclooxygenase-2 (COX-2) expression 1. Here, we explored the mechanisms for activation of apoptosis, evaluated the impact on inflammatory genes in a broader panel of cells and tested whether topical anti-inflammatory effects could be observed in vivo.

Methods and results: TF-2 triggered apoptosis in five other transformed cancer cell lines, inducing cell shrinkage, membrane blebbing, and mitochondrial clustering within 3 h of treatment. Among a set of pro-apoptotic genes, TF-2 quickly induced the up-regulation of P53 and BAX, suggesting mitochondria as the primary target. Using a cell model for inflammatory response, we showed that TF-2 suppressed the 12-O-tetradecanoylphorbol-13-acetate-induced COX-2 gene expression, and also down-regulated TNF-α, iNOS, ICAM-1, and NFκB. A reporter gene assay showed that TF-2 down-regulated COX-2 at the transcriptional level. We also demonstrated that TF-2 exhibited anti-inflammatory activity in two mouse models of inflammation. Topical application with TF-2 significantly reduced ear edema and produced a pattern of gene down-regulation similar to that observed in the cell model.

Conclusion: These results suggest that the anti-inflammatory and pro-apoptotic activity of TF-2 may be exploited therapeutically in cancer and other diseases associated with inflammation.

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