Effects of Pre- and Post-Supplementation of Taurine in the Hippocampus of a Gerbil Model of Transient Global Cerebral Ischemia.

Taurine is a free amino acid with various effects, such as developing the nervous system, an immune function, an antioxidative effect, enhancing muscle and cardiovascular function, and reducing fatigue. In this study, we investigated the effect of taurine supplementation on ischemic neuronal damage in the hippocampus of gerbils. Taurine (150 mg/kg) was orally administered to gerbils before and after induction of transient ischemia. Histologically, we examined surviving and degenerating neurons by neuronal nuclei immunostaining and fluoro-jade C (FJC) staining. Gliosis was morphologically confirmed by GFAP and Iba1 immunostaining. Compared to the ischemia and pre-treated gerbils, pre- and post-taurine supplementation was neuroprotective by maintaining higher number of mature NeuN-immunoreactive neurons and reducing neuronal death (FJC-stained cells) in the hippocampal CA1 region. Additionally, the ischemia-induced reactive astrocytosis and microgliosis was significantly mitigated by long-term taurine treatment in the gerbil hippocampus. Furthermore, we confirmed that pre- and post-taurine supplementation downregulated ischemia-mediated induction in the MAPK cascade, such as ERK, JNK, and p38, which are involved in oxidative stress, inflammation, apoptosis, and cell differentiation, and this treatment upregulated an ischemia-mediated reduction in antioxidants such as SOD2, GPX4, and anti-apoptotic factor Bcl-2 in the gerbil hippocampus. Pre- and post-taurine supplementation also downregulated again the ischemic injury-mediated activation of transcriptional factor NFkβ, an important gene expression regulator, especially in the inflammatory response, and pro-apoptotic factor Bax in the gerbil hippocampus. Our present results suggest that pre- and post-taurine supplementation has potential in neuroprotection against ischemia-induced neuronal death and glial activation by attenuating oxidative stress and apoptosis.