作者: Hai Chen , Hideyuki Yoshioka , Gab Seok Kim , Joo Eun Jung , Nobuya Okami
关键词: Oxidative stress 、 Neuroprotection 、 Superoxide dismutase 、 NADPH oxidase 、 Pharmacology 、 Brain damage 、 Ischemia 、 Mitochondrion 、 Biology 、 Biochemistry 、 Programmed cell death
摘要: Abstract Significant amounts of oxygen free radicals (oxidants) are generated during cerebral ischemia/reperfusion, and oxidative stress plays an important role in brain damage after stroke. In addition to oxidizing macromolecules, leading cell injury, oxidants also involved death/survival signal pathways cause mitochondrial dysfunction. Experimental data from laboratory animals that either overexpress (transgenic) or deficient (knock-out) antioxidant proteins, mainly superoxide dismutase, have provided strong evidence the ischemic damage. mitochondria, recent reports demonstrate NADPH oxidase (NOX), pro-oxidant enzyme, is generation Inhibition NOX neuroprotective against ischemia. We propose dismutase activity a major determinant for damage/repair these anti- pro-oxidan...