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

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.