Protective Effect of PineXol®on Hydrogen Peroxide-induced Apoptosis on SK-N-MC Cells and Focal Ischemia Rodent Models

The purpose of this study was to evaluate the protective effect of <TEX>PineXol(R)</TEX> on <TEX>H₂O₂</TEX>-induced cell death in SK-N-MC cells, and in early stage focal ischemia rodent model. SK-N-MC cells were pre-treated with <TEX>200μM</TEX> <TEX>H₂O₂</TEX> or various concentrations of <TEX>PineXol(R)</TEX> (10, 30, and 50 pg/mL) for 24 h, and then exposed to <TEX>H₂O₂</TEX> for 3 h. Cell death was assessed by the CCK-8 assay, reactive oxygen species (ROS) assay, and lactate and dehydrogenase (LDH) release assay. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) expressions were also analyzed by western blotting. Focal ischemia rodent model was used as the in vivo model, and different concentrations of <TEX>PineXol(R)</TEX> (1, 10, and 100 mg/kg) were administered. One week after administration, reduction of infarct volume was analyzed by TTC staining. Cell viability of <TEX>H₂O₂</TEX>-treated SK-N-MC cells significantly increased by pre-treatment of <TEX>PineXol(R)</TEX> (p<0.05). <TEX>PineXol(R)</TEX> pre-treatment also induced significant decrease of ROS and LDH expressions. However, <TEX>PineXol(R)</TEX> did not affect the infarct volume. These results suggest that <TEX>PineXol(R)</TEX> has significant neuroprotective effect in vitro, but statistical significance was not confirmed in the in vivo focal ischemia model.