| Objective: To investigate the effects of ischemic postconditioning on braininjury and protein oxidization in focal ischemia and reperfusion.Methods: All the animals were divided randomly into sham-operated group,ischemia group and ischemic postconditioning group. Ischemia was produced byusing middle cerebral artery occlusion (MCAO), and ischemic post-conditioning wasperformed by using3cycles of30-second/30-second reperfusion/re-occlusion at theend of2hours ischemia. Brain infarction size was evaluated by TTC staining. Thelevel of H2O2was measured fluorimetrically by monitoring the oxidation ofp-hydroxy phenyl acetate coupled with enzymatic reduction of hydrogen peroxide byhorseradish peroxidase. Activities of superoxide dismutase and catalase wereassayed by using commercial kits. Proteasome activity, protein carbonyl derivativesand advanced oxidized protein products were measured spectrophotometrically. Allthe data are expressed as Mean±SD and analyzed statistically.Results: Ischemic postconditioning made the size of brain infarction decreasefrom37.91%±2.16%to21.38%±1.65%(p<0.01), concomitant with significantreduction in the levels of protein carbonyl products and advanced oxidation proteinproducts from15.61±1.92mmol/mg protein and11.64±1.92mmol/mg protein to11.71±1.37mmol/mg protein and9.12±1.27mmol/mg protein, respectively. Bycontrast, activities of SOD and CAT were elevated respectively by ischemicpostconditioning from78.45±1.62U/g protein and8.76±1.33U/g to96.24±11.37U/g protein and12.56±2.14U/g protein, as well as proteasome activity increased from65.22%±7.31%to84.63%±11.24%.Conclusion: Our study indicates that the reduction of brain infarct size isbenefited from the decreased protein oxidization due to ischemic postconditioning,and protein oxidization is a potential target for preventing cerebral injury. |
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