Abstract
ABSTRACTOxidative stress can be induced neurotoxic insults by increasing intracellular H2O2, which has been implicated in various neurodegenerative diseases in aging. We investigated the mechanism by which Debo protects PC12 cells from serum deprivation-induced apoptosis. PC12 cells underwent apoptotic death in association with increase in caspase 3-like activity, DNA fragmentation, H2O2 production, GSH depletion, and NF-κB activation after 24 hr of serum withdrawal. Debo protected cells from a serum deprivation-induced cytotoxicity in a dose dependent manner. Debo recovered the intracellular GSH level decreased by serum deprivation in PC12 cells. Also, Debo inhibited the activation of caspase 3-like protease of serum-deprived PC12 cells in a dose dependent manner. Furthermore, Debo inhibited the transcriptional activation of NF-κB by serum deprivation. These findings indicate that Debo may protect PC12 cells against apoptosis by serum deprivation via generation of intracellular GSH to scavenge oxidative radicals including H2O2.
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