• Ann. N. Y. Acad. Sci. · May 2005

    Oxidative toxicity in BV-2 microglia cells: sesamolin neuroprotection of H2O2 injury involving activation of p38 mitogen-activated protein kinase.

    • Rolis Chien-Wei Hou, Chia-Chuan Wu, Jing-Rong Huang, Yuh-Shuen Chen, and Kee-Ching G Jeng.
    • Jen-Teh Junior College of Medical and Nursing Management, Miaoli, Taiwan.
    • Ann. N. Y. Acad. Sci. 2005 May 1;1042:279-85.

    AbstractReactive oxygen species (ROS) has been proposed to play a pathogenic role in neuronal injury. Sesame antioxidants that inhibit lipid peroxidation and regulate cytokine production may suppress ROS generation. In this study, we focused on the effect of sesamolin on H2O2-induced neurotoxicity and ROS production in the murine microglial cell line BV-2. Results indicate that the H2O2 elicited BV-2 cell death in a concentration- and time-dependent manner. ROS generation in BV-2 cells was time-dependently increased by the H2O2 treatment. Sesamolin reduced ROS generation in BV-2 cells. p38 mitogen-activated protein kinase (MAPK) and caspase-3 were also activated in BV-2 cells under H2O2 stress. Sesamolin was able to inhibit H2O2-induced p38 MAPK and caspase-3 activation and cell death. In addition, sesamolin preserved superoxide dismutase and catalase activities in BV-2 cells under H2O2 stress. In conclusion, sesamolin protects microglia against H2O2-induced cell injury and this protective effect was accompanied by its inhibition of p38 MAPK and caspase-3 activation and ROS production.

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