Nobuya Okami

TL;DR: It is proposed that superoxide dismutase and NOX activity in the brain is a major determinant for ischemic damage/repair and that these major anti- and pro-oxidant enzymes are potential endogenous molecular targets for stroke therapy.

TL;DR: Although the mechanisms of cell death after cerebral ischemia remain unclear, mitochondria obviously play a role by activating signaling pathways through ROS production and by regulating mitochondria-dependent apoptosis pathways.

TL;DR: This study has developed a focal stroke model using mice deficient in mitochondrial manganese-superoxide dismutase (SOD2−/+) to investigate neurovascular endothelial damage that occurs during reperfusion and identified the signal transducer and activator of transcription 3 (STAT3) as a transcription factor of the mouse SOD2 gene.

TL;DR: It is speculated that Hb-induced oxidative stress may contribute to early BBB dysfunction and subsequent apoptosis, partly through MMP activation, and that SOD1 overexpression may reduce H b- induced oxidative stress,BBB dysfunction, and apoptotic cell death.

TL;DR: The role of NOX2 in post-ischemic cerebral inflammation is investigated using a transient middle cerebral artery occlusion model in mice and it is demonstrated thatNOX2 inhibition provides neuroprotection against inflammatory cytokine-mediated brain damage.