Oxidative Toxicity in BV-2 Microglia Cells: Sesamolin Neuroprotection of H_2O_2 Injury Involving Activation of p38 Mitogen-Activated Protein Kinase

摘要

Reactive oxygen species (ROS) has been proposed to play a pathogenic role in neuronal injury. Sesame antioxidants that inhibit lipid peroxida-tion and regulate cytokine production may suppress ROS generation. In this study, we focused on the effect of sesamolin on H_2O_2-induced neurotoxicity and ROS production in the murine microglial cell line BV-2. Results indicate that the H_2O_2 elicited BV-2 cell death in a concentration- and time-dependent manner. ROS generation in BV-2 cells was time-dependently increased by the H_2O_2 treatment. Sesamolin reduced ROS generation in BV-2 cells. p38 mito-gen-activated protein kinase (MAPK) and caspase-3 were also activated in BV-2 cells under H_2O_2 stress. Sesamolin was able to inhibit H_2O_2-induced p38 MAPK and caspase-3 activation and cell death. In addition, sesamolin preserved superoxide dismutase and catalase activities in BV-2 cells under H_2O_2 stress. In conclusion, sesamolin protects microglia against H_2O_2-induced cell injury and this protective effect was accompanied by its inhibition of p38 MAPK and caspase-3 activation and ROS production.