Oxidative stress-associated impairment of proteasome activity during ischemia-reperfusion injury.

摘要: Numerous studies indicate a role for oxidative stress in the neuronal degeneration and cell death that occur during ischemia–reperfusion injury. Recent data suggest inhibition of proteasome may be means by which mediates death. In current study, authors demonstrate there is time-dependent decrease activity, not associated with decreased expression subunits, after cerebral To determine mediating inhibition, were conducted mice either overexpressed antioxidant enzyme glutathione peroxidase [GPX 1(+)], or devoid activity (GPX −/−). After ischemia–reperfusion, GPX 1(+) displayed infarct size, attenuated neurologic impairment, reduced levels compared −/− wild type mice. addition, lower le...