Skip to main content

Advertisement

SpringerLink
Log in

Black tea polyphenol theaflavin suppresses LPS-induced ICAM-1 and VCAM-1 expression via blockage of NF-κB and JNK activation in intestinal epithelial cells

  • Original Research Paper
  • Published:
Inflammation Research Aims and scope Submit manuscript

Abstract

Objective

The aim of this study was to determine the impact of the black tea polyphenol, theaflavin, on the expression of adhesion molecules and activation of lipopolysaccharide (LPS)-induced innate signaling in rat intestinal epithelial (RIE) cells.

Methods

The effect of theaflavin on neutrophil adhesion, expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, LPS-induced nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) signaling was examined by neutrophil adhesion assay, RT-PCR, Western blotting, immunofluorescence, and electrophoretic mobility shift assay (EMSA).

Results

Theaflavin suppressed adhesion of neutrophils to LPS-stimulated RIE cells. LPS-induced ICAM-1 and VCAM-1 expressions were inhibited by theaflavin. LPS-induced IκBα phosphorylation/degradation and nuclear translocation of NF-κB/p65 were blocked by theaflavin. Also, theaflavin blocked NF-κB DNA-binding activity in EMSA. LPS-induced phosphorylation of JNK was inhibited by theaflavin. Bay11-7082 (a NF-κB inhibitor) and SP600125 (a JNK inhibitor) suppressed the LPS-induced ICAM-1 and VCAM-1 mRNA accumulations.

Conclusions

These results indicate that black tea polyphenol theaflavin suppresses LPS-induced ICAM-1 and VCAM-1 expressions through blockage of NF-κB and JNK activation in intestinal epithelial cells.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1
Fig. 2
Fig. 3
Fig. 4
Fig. 5
Fig. 6

Similar content being viewed by others

References

  1. Calixto JB, Campos MM, Otuki MF, Santos AR. Anti-inflammatory compounds of plant origin. Part II. modulation of pro-inflammatory cytokines, chemokines and adhesion molecules. Planta Med. 2004;70:93–103.

    Article  PubMed  CAS  Google Scholar 

  2. Lin JK. Cancer chemoprevention by tea polyphenols through modulating signal transduction pathways. Arch Pharm Res. 2002;25:561–71.

    Article  PubMed  CAS  Google Scholar 

  3. Sarkar FH, Li Y, Wang Z, Kong D. Cellular signaling perturbation by natural products. Cell Signal. 2009;21:1541–7.

    Article  PubMed  CAS  Google Scholar 

  4. Khan N, Mukhtar H. Tea polyphenols for health promotion. Life Sci. 2007;81:519–33.

    Article  PubMed  CAS  Google Scholar 

  5. Khan N, Mukhtar H. Multitargeted therapy of cancer by green tea polyphenols. Cancer Lett. 2008;269:269–80.

    Article  PubMed  CAS  Google Scholar 

  6. Butt MS, Sultan MT. Green tea: nature’s defense against malignancies. Crit Rev Food Sci Nutr. 2009;49:463–73.

    Article  PubMed  CAS  Google Scholar 

  7. Chen D, Milacic V, Chen MS, Wan SB, Lam WH, Huo C, et al. Tea polyphenols, their biological effects and potential molecular targets. Histol Histopathol. 2008;23:487–96.

    PubMed  Google Scholar 

  8. Sharma V, Rao LJ. A thought on the biological activities of black tea. Crit Rev Food Sci Nutr. 2009;49:379–404.

    Article  PubMed  CAS  Google Scholar 

  9. Aneja R, Odoms K, Denenberg AG, Wong HR. Theaflavin, a black tea extract, is a novel anti-inflammatory compound. Crit Care Med. 2004;32:2097–103.

    Article  PubMed  CAS  Google Scholar 

  10. Ukil A, Maity S, Das PK. Protection from experimental colitis by theaflavin-3,3′-digallate correlates with inhibition of IKK and NF-kappaB activation. Br J Pharmacol. 2006;149:121–31.

    Article  PubMed  CAS  Google Scholar 

  11. Gosslau A, En Jao DL, Huang MT, Ho CT, Evans D, Rawson NE, et al. Effects of the black tea polyphenol theaflavin-2 on apoptotic and inflammatory pathways in vitro and in vivo. Mol Nutr Food Res. 2010;54:1–11.

    Google Scholar 

  12. Cai F, Li C, Wu J, Min Q, Ouyang C, Zheng M, et al. Modulation of the oxidative stress and nuclear factor kappaB activation by theaflavin 3,3′-gallate in the rats exposed to cerebral ischemia–reperfusion. Folia Biol (Praha). 2007;53:164–72.

    CAS  Google Scholar 

  13. Huang MT, Liu Y, Ramji D, Lo CY, Ghai G, Dushenkov S, et al. Inhibitory effects of black tea theaflavin derivatives on 12-O-tetradecanoylphorbol-13-acetate-induced inflammation and arachidonic acid metabolism in mouse ears. Mol Nutr Food Res. 2006;50:115–22.

    Article  PubMed  CAS  Google Scholar 

  14. Zhao J, Jin X, Yaping E, Zheng ZS, Zhang YJ, Athar M, et al. Photoprotective effect of black tea extracts against UVB-induced phototoxicity in skin. Photochem Photobiol. 1999;70:637–44.

    Article  PubMed  CAS  Google Scholar 

  15. Shih DQ, Targan SR. Insights into IBD pathogenesis. Curr Gastroenterol Rep. 2009;11:473–80.

    Article  PubMed  Google Scholar 

  16. Hörmannsperger G, Haller D. Molecular crosstalk of probiotic bacteria with the intestinal immune system: clinical relevance in the context of inflammatory bowel disease. Int J Med Microbiol. 2010;300:63–73.

    Article  PubMed  Google Scholar 

  17. Strober W, Fuss I, Mannon P. The fundamental basis of inflammatory bowel disease. J Clin Invest. 2007;117:514–21.

    Article  PubMed  CAS  Google Scholar 

  18. Podolsky DK, Xavier RJ. Unravelling the pathogenesis of inflammatory bowel disease. Nature. 2007;448:427–34.

    Article  PubMed  Google Scholar 

  19. Sartor RB. Microbial influences in inflammatory bowel diseases. Gastroenterology. 2008;134:577–94.

    Article  PubMed  CAS  Google Scholar 

  20. Li Y, Tian Y, Yu C, Zhu W, Li J. A systematic review and meta-analysis of anti-adhesion molecule therapy in patients with active Crohn’s disease. Scand J Gastroenterol. 2009;44:1435–42.

    Article  PubMed  CAS  Google Scholar 

  21. Rivera-Nieves J, Gorfu G, Ley K. Leukocyte adhesion molecules in animal models of inflammatory bowel disease. Inflamm Bowel Dis. 2008;14:1715–35.

    Article  PubMed  Google Scholar 

  22. Danese S, Semeraro S, Marini M, Roberto I, Armuzzi A, Papa A. Adhesion molecules in inflammatory bowel disease: therapeutic implications for gut inflammation. Dig Liver Dis. 2005;37:811–8.

    Article  PubMed  CAS  Google Scholar 

  23. Vainer B. Intercellular adhesion molecule-1 (ICAM-1) in ulcerative colitis: presence, visualization, and significance. Inflamm Res. 2005;54:313–27.

    Article  PubMed  CAS  Google Scholar 

  24. Rutgeerts P, Van Deventer S, Schreiber S. Review article: the expanding role of biological agents in the treatment of inflammatory bowel disease—focus on selective adhesion molecule inhibition. Aliment Pharmacol Ther. 2003;17:1435–50.

    Article  PubMed  CAS  Google Scholar 

  25. Sanchez-Munoz F, Dominguez-Lopez A, Yamamoto-Furusho JK. Role of cytokines in inflammatory bowel disease. World J Gastroenterol. 2008;14:4280–8.

    Article  PubMed  CAS  Google Scholar 

  26. Karrasch T, Jobin C. NF-κB and the intestine: friend or foe? Inflamm Bowel Dis. 2007;14:114–24.

    Article  Google Scholar 

  27. Perkins ND, Gilmore TD. Good cop, bad cop: the different faces of NF-κB. Cell Death Differ. 2006;13:759–72.

    Article  PubMed  CAS  Google Scholar 

  28. Hayden MS, Ghosh S. Signaling to NF-κB. Genes Dev. 2004;18:2195–224.

    Article  PubMed  CAS  Google Scholar 

  29. Broom OJ, Widjaya B, Troelsen J, Olsen J, Nielsen OH. Mitogen activated protein kinases: a role in inflammatory bowel disease? Clin Exp Immunol. 2009;158:272–80.

    Article  PubMed  CAS  Google Scholar 

  30. Wei J, Feng J. Signaling pathways associated with inflammatory bowel disease. Recent Pat Inflamm Allergy Drug Discov. 2010;4:105–17.

    Article  PubMed  CAS  Google Scholar 

  31. Van Den Blink B, Ten Hove T, Van Den Brink GR, Peppelenbosch MP, Van Deventer SJ. From extracellular to intracellular targets, inhibiting MAP kinases in treatment of Crohn’s disease. Ann N Y Acad Sci. 2002;973:349–58.

    Article  Google Scholar 

  32. Burns RC, Rivera-Nieves J, Moskaluk CA, Matsumoto S, Cominelli F, Ley K. Antibody blockade of ICAM-1 and VCAM-1 ameliorates inflammation in the SAMP-1/Yit adoptive transfer model of Crohn’s disease in mice. Gastroenterology. 2001;121:1428–36.

    Article  PubMed  CAS  Google Scholar 

  33. Lin YL, Tsai SH, Lin-Shiau SY, Ho CT, Lin JK. Theaflavin-3,3′-digallate from black tea blocks the nitric oxide synthase by down-regulating the activation of NF-kappaB in macrophages. Eur J Pharmacol. 1999;367:379–88.

    Article  PubMed  CAS  Google Scholar 

  34. Nomura M, Ma W, Chen N, Bode AM, Dong Z. Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced NF-kappaB activation by tea polyphenols (–)-epigallocatechin gallate and theaflavins. Carcinogenesis. 2000;21:1885–90.

    Article  PubMed  CAS  Google Scholar 

  35. Marcu KB, Otero M, Olivotto E, Borzi RM, Goldring MB. NF-kappaB signaling: multiple angles to target OA. Curr Drug Targets. 2010;11:599–613.

    Article  PubMed  CAS  Google Scholar 

  36. Liang Y, Zhou Y, Shen P. NF-kappaB and its regulation on the immune system. Cell Mol Immunol. 2004;1:343–50.

    PubMed  CAS  Google Scholar 

  37. Kaminska B. MAPK signalling pathways as molecular targets for anti-inflammatory therapy—from molecular mechanisms to therapeutic benefits. Biochim Biophys Acta. 2005;1754:253–62.

    PubMed  CAS  Google Scholar 

  38. Kułdo JM, Ogawara KI, Werner N, Asgeirsdóttir SA, Kamps JA, Kok RJ, et al. Molecular pathways of endothelial cell activation for (targeted) pharmacological intervention of chronic inflammatory diseases. Curr Vasc Pharmacol. 2005;3:11–39.

    Article  PubMed  Google Scholar 

Download references

Acknowledgments

This work was supported by a grant (0720570) from the National R&D Program for Cancer Control, Ministry of Health and Welfare, Republic of Korea, and partly by a grant from the Korea Science and Engineering Foundation through the Medical Research Center for Gene Regulation (R13-2002-013-04001-0) at Chonnam National University, Republic of Korea.

Conflict of interest

None declared.

Author information

Authors and Affiliations

  1. Department of Internal Medicine, Chonnam National University Medical School, 8 Hak-Dong, Dong-ku, 501-757, Gwangju, Korea

    Young-A Song, Young-Lan Park, Sun-Hye Yoon, Kyu-Yeol Kim, Sung-Bum Cho, Wan-Sik Lee, Ik-Joo Chung & Young-Eun Joo

Authors
  1. Young-A Song
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Young-Lan Park
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Sun-Hye Yoon
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Kyu-Yeol Kim
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Sung-Bum Cho
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Wan-Sik Lee
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Ik-Joo Chung
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Young-Eun Joo
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Young-Eun Joo.

Additional information

Responsible Editor: Liwu Li.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Song, YA., Park, YL., Yoon, SH. et al. Black tea polyphenol theaflavin suppresses LPS-induced ICAM-1 and VCAM-1 expression via blockage of NF-κB and JNK activation in intestinal epithelial cells. Inflamm. Res. 60, 493–500 (2011). https://doi.org/10.1007/s00011-010-0296-z

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00011-010-0296-z

Keywords

Search

Navigation