PROTECTIVE EFFECTS OF DEBO ON ZINC-INDUCED APOPTOSIS OF C6 GLIAL CELLS VIA MODULATION OF INTRACELLULAR ANTIOXIDANT, REDUCED GLUTATHIONE

Abstract

In the present study, the mechanical basis of a traditional herbal prescription, Debo, on cytotoxic damage of the brain cells including C6 glial and PC12 cells has been studied. Traditionally, Debo has been employed for the purpose of preventing responses to trauma, ischemia, and other diseases in the nervous system. C6 glial cells were exposed to oxidative stress through the imployment of ZnCl₂, and generates H₂O₂ and hydroxyl radicals by fenton reaction. ZnCl₂-induced death of C6 glial cells, which was revealed as apoptosis by chromatin condensation as well as DNA fragmentation. Pretreatment of Debo significantly prevented apoptotic death of C6 glial cells via inhibition of H₂O₂ generation as well as the recovering of an antioxidant, reduced glutathione (GSH). Also, deprivation of serum and glucose, found in ischemia, deceased the viability of PC12 cells up to 60% via generation of H₂O₂. However, Debo significantly protected cells from ischemic damage through decrease in H₂O₂ generation. Furthermore, Debo markedly inhibited the transcriptional activation of NF-κB by ZnCl₂ in C6 glial cells. These results suggest that Debo may function as an antioxidant system against free radicals and be applicable to protect brain cells against oxidative or ischemic stresses.