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Interplay between ischemic stroke and Nrf2. Ischemia-reperfusion leads to increased levels of oxidants (i.e., hydrogen peroxide (H2O2), superoxide anion (O2•−)) that, in turn, can activate Nrf2. Nrf2-downstream proteins (i.e., heme oxygenase-1 (HO-1), superoxide dismutase (SOD)) can mitigate the deleterious effects of oxidants produced in excess during IR, preventing oxidative stress and cell death.
