Fullerenol Nanoparticles Decrease Brain Infarction Through Potentiation of Superoxide Dismutase Activity During Cerebral Ischemia-Reperfusion Injury
Ithasbeendemonstratedthatweakening of thebrainantioxidant systemandoxidative stress is themaincontributor in pathophysiology of ischemic stroke.
Since fullerenol nanoparticles have powerful antioxidant effects in biological environments, we aimed to evaluate whether fullerenol administration during cerebral ischemia potentiates the antioxidant defense systemof ischemic brain and de- creases cerebral infarction.
Thirty six rats were randomly divided into three groups (n = 12 for each group): sham, control ischemia and ischemic treatment groups. Themiddle cerebral artery (MCA) was obstructed for 90minutes in right hemispheres of control ischemia and ischemic treatment groups to achieve the experimentalmodel of ischemic stroke. Treated rats received fullerenol nanoparticles (10 mg/kg, intraperitoneally) 30minutes beforeMCA occlusion. Brain infarction, glutathione content and superoxide dismutase (SOD) activity were determined at the end of experiment.
Occlusion of MCA induced considerable infarction and lesion in ischemic hemispheres of control ischemic rats (52759 mm3 ) in accompany with a decrease in the glutathione content (45%), and SOD activity (29%) compared with sham rats. Adminis- tration of fullerenol in ischemic treatment group before MCA occlusion reduced the value of infarction (138 67 mm3 ) and also increased the value of the SOD activity by 33% compared to control ischemic group.
Our findings indicate that fullerenol nanoparticles decrease the brain infarction through enhancement of the SOD activity during cerebral ischemia-reperfusion injury.
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