Nutrition Research
Volume 25, Issue 5 , Pages 477-483, May 2005

Green tea polyphenols suppress nitric oxide–induced apoptosis and acetylcholinesterase activity in human neuroblastoma cells

  • Joo Ho Chung

      Affiliations

    • Department of Pharmacology, College of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea
    • ,
  • Mujo Kim

      Affiliations

    • Pharma Foods International, Minami-ku, Kyoto 601-8357, Japan
    • ,
  • Hye Kyung Kim

      Affiliations

    • Department of Food and Biotechnology, Hanseo University, Seosan 356-706, Republic of Korea
    • Corresponding Author InformationCorresponding author. Tel.: +82 41 660 1454; fax: +82 41 660 1119.

Received 14 December 2003; received in revised form 8 October 2004; accepted 3 February 2005.

Abstract 

Oxidative stress is a main mediator in nitric oxide (NO)–induced neurotoxicity and has been implicated in the pathogenesis of many neurodegenerative disorders. Green tea polyphenols (GTPs) exert a wide range of biochemical and pharmacological effects and have been shown to prevent oxidative stress–related diseases. This paper demonstrated that GTP protected the neurotoxicity of NO, generated by S-nitroso-N-acetylpenicillamine, in human neuroblastoma cells. Green tea polyphenols attenuated the NO-induced apoptotic cell death, assessed by cell viability, Hoechst staining, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining. The protective mechanism was via elevated expression of the antiapoptotic bcl-2 gene and suppressed expression of the proapoptotic bax gene, thereby arresting NO-induced apoptotic cell death. Furthermore, GTP appeared to be a potent inhibitor of acetylcholinesterase, exhibiting an IC50 of 248 μg/mL. To our knowledge, this is the first report showing the inhibitory effect of GTP on acetylcholinesterase activity, exploiting potential use in neurodegenerative disease.

Keywords: Tea polyphenols, Nitric oxide, Human neuroblastoma cells, Apoptosis, Acetylcholinesterase, Neurodegenerative disease

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PII: S0271-5317(05)00052-7

doi:10.1016/j.nutres.2005.02.002

Nutrition Research
Volume 25, Issue 5 , Pages 477-483, May 2005

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