抄録
Previous studies have demonstrated that DNA injury occurs in the brain after intracerebral hemorrhage (ICH) due to the release of iron from hemoglobin. We, therefore, examined whether edaravone, free radical scavenger, can reduce ICH-induced brain injury. Animal protocols were approved by the Animal Committee of the Kagawa University. Pentobarbital anesthetized male Sprague-Dawley rats were anesthetized received an infusion of 100-μl autologous whole blood into the right basal ganglia or just a needle insertion (shams). The rats were sacrificed 24 hours later. In the first set of experiments, iron distribution was examined histochemically (enhanced Perl's reaction). In the second set, apurnic/apyrimidinic abasic sites (AP-sites) and 8-Hydroxyl-2'-deoxyguanosine (8-OHdG), which are hallmarks of DNA oxidation, were investigated by AP-sites assay and immunohistochemistry after treatment for ICH (n=5). Iron accumulation was observed in the perihematomal zone 24 hours after ICH. Edaravone attenuated ICH-induced changes in AP-sites and 8-OHdG (respectinely, P<0.05). Iron accumulation occurs in the brain after ICH and edaravone attenuates ICH-induced oxidative injury suggesting that free radical scavenger may be potential therapeutic agents for ICH. [J Physiol Sci. 2008;58 Suppl:S216]
