作者: Jie Zhang , Yunyi Hong , Wei Cao , Shankai Yin , Haibo Shi
关键词: Enzyme 、 Nicotinamide adenine dinucleotide 、 Cell biology 、 Glutathione 、 Adenosine 、 MAPK/ERK pathway 、 NAD+ kinase 、 SIRT2 、 Chemistry 、 Oxidative phosphorylation
摘要: NAD+ (oxidized form of nicotinamide adenine dinucleotide) administration is highly beneficial in numerous models diseases and aging. It becoming increasingly important to determine if treatment may directly increase the antioxidant capacity cells under basal conditions. In current study, we tested our hypothesis that can enhance conditions by using PC12 as a cellular model. We found GSH/GSSG ratios also both mRNA protein level γ-glutamylcysteine ligase (γ-GCL)-a key enzyme for glutathione synthesis, which appears be mediated NAD+-induced Nrf2 activity. These changes prevented SIRT2 siRNA inhibitor AGK2. The blocked ERK signaling U0126. Moreover, activation Collectively, study has provided first evidence conditions, SIRT2, ERK, Nrf2. findings have suggested not only great nutritional potential NAD+, but novel mechanism underlying protective effects disease models: resistance normal oxidative insults increasing cells.