绿原酸
神经保护
活性氧
氧化应激
生物化学
化学
抗氧化剂
咖啡因
细胞凋亡
药理学
生物
食品科学
内分泌学
作者
Jiyoung Kim,Siyoung Lee,Jaesung Shim,Hyo Won Kim,Jaekyoon Kim,Young Jin Jang,Hee Seok Yang,Ji‐Man Park,Seung Hwan Choi,Ji Hye Yoon,Ki Won Lee,Hyong Joo Lee
标识
DOI:10.1016/j.neuint.2012.02.004
摘要
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.
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