Taurine Chloramine Prevents Neuronal HT22 Cell Damage Through Nrf2-Related Heme Oxygenase-1.

Abstract

Oxidative cell damages are able to contribute to neuronal degeneration in several diseases of the central nervous system (CNS) including stroke as well as ischemia. Heme oxygenase (HO)-1 plays a major role in the pathogenesis of neuronal disorder. Taurine chloramine (TauCl) has been shown to possess strong neuronal activities; however, the direct effects of TauCl on neuronal cell death remain to be determined. Therefore, this study was designed to assess the neuroprotective effect of TauCl using oxidative stress-stimulated mouse hippocampal HT22 cells. TauCl showed protective effects against oxidative stress-induced neurotoxicity and inhibited the reactive oxygen species (ROS) production by inducing the heme oxygenase (HO)-1 expression in HT22 cells. TauCl upregulated HO-1 expression and it also increased the nuclear factor E2-related factor 2 (Nrf2) translocation to nuclear. Using an inhibitor of HO-1 activity, we verified that the oxidative stress-related HT22 cell death was significantly suppressed by TauCl. In addition, we found reduced TauCl-induced HO-1 expression and cytoprotection following treatment of the cells with an extracellular signal-regulated kinase (ERK) inhibitor (PD98059) or a p38 inhibitor (SB203580), but not following treatment with a SP600125 as a c-Jun NH2-terminal kinase (JNK) inhibitor. These findings suggest that TauCl improves cellular damage induced by glutamate or H2O2 through ERK and p38, Nrf2, and HO-1 pathways in HT22 cells.