Forskning

February 24, 2012

Caffeinated coffee, decaffeinated coffee, and the phenolic phytochemical chlorogenic acid up-regulate NQ01 expression and prevent H2o2 induced apoptosis in primary cortical neurons

J Kim et al, Caffeinated coffee, decaffeinated coffee, and the phenolic phytochemical chlorogenic acid up-regulate NQ01 expression and prevent H2o2 induced apoptosis in primary cortical neurons, Neurochemistry International, 2012 

ABSTRACT:

Neurodegenerative disorders are strongly associated with oxidative stress, which is induced by reactive oxygen species including hydrogen peroxide (H2O2). Epidemiological studies have suggested that coffee  may be neuroprotective, but the molecular mechanisms underlying this effect have not been clarified. In  this study, we investigated the protective effects of caffeinated coffee, decaffeinated coffee, and the phenolic phytochemical chlorogenic acid (5-O-caffeoylquinic acid), which is present in both caffeinated and decaffeinated coffee, against oxidative neuronal death. H2O2-induced apoptotic nuclear condensation in  neuronal cells was strongly inhibited by pretreatment with caffeinated coffee, decaffeinated coffee, or  chlorogenic acid. Pretreatment with caffeinated coffee, decaffeinated coffee, or chlorogenic acid inhibited the H2O2-induced down-regulation of anti-apoptotic proteins Bcl-2 and Bcl-XL while blocking H2O2-  induced pro-apoptotic cleavage of caspase-3 and pro-poly(ADP-ribose) polymerase. We also found that  caffeinated coffee, decaffeinated coffee, and chlorogenic acid induced the expression of NADPH:quinine  oxidoreductase 1 (NQO1) in neuronal cells, suggesting that these substances protect neurons from  H2O2-induced apoptosis by up-regulation of this antioxidant enzyme. The neuroprotective efficacy of  caffeinated coffee was similar to that of decaffeinated coffee, indicating that active compounds present  in both caffeinated and decaffeinated coffee, such as chlorogenic acid, may drive the effects.