Abstract
Glutamate-induced oxidative neurotoxicity plays a part role in neuronal degeneration on the disorders of central nervous system (CNS). The expression of heme oxygenase (HO)-1 mediated by Inducible nuclear factor-E2-related factor 2 (Nrf2) functions as an anti-oxidants that is able to play an important role in the pathogenesis of several neuronal disorders. In the present study, taurine showed the inhibitory effect against reactive oxygen species (ROS) induction and protective effects against neurotoxicity induced by glutamate- and H2O2 through induction of HO-1 expression in HT22 cells. Moreover, taurine promoted the Nrf2 nuclear translocation in HT22 cells. We also verified the oxidative stress-mediated cell death of HT22 cells was significantly repressed by taurine, using tin protoporphyrin (SnPP) as an HO activity inhibitor. In addition, we found that treatment of the cells with p38 inhibitor (SB203580) suppressed taurine-induced HO-1 expression and cytoprotection, but inhibitors of c-Jun NH2 terminal kinase (JNK) (SP600125) or extracellular signal regulated kinase (ERK) (PD98059) did not. These results suggest that taurine improves the resistance against oxidative damages induced by glutamate in HT22 cells via the p38/Nrf2-dependent HO-1 expression. Our results demonstrated the potential application of taurine as a therapeutic agent for neurodegenerative diseases.
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