Author/Authors :
Darabi، Shamsi نويسنده Department of Physiology and Biophysics, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran , , Mohammadi، Mohammad Taghi نويسنده Department of Physiology and Biophysics, School of Medicine, Baqiyatallah University of Medical Sciences, Tehran, IR Iran , , Sobhani، Zeinab Sadat نويسنده Department of Physiology and Biophysics, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran ,
Abstract :
It has been demonstrated that weakening of the brain antioxidant system and oxidative stress is the main contributor 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 system of ischemic brain and decreases cerebral infarction. Thirty six rats were randomly divided into three groups (n = 12 for each group): sham, control ischemia and ischemic treatment groups. The middle cerebral artery (MCA) was obstructed for 90 minutes in right hemispheres of control ischemia and ischemic treatment groups to achieve the experimental model of ischemic stroke. Treated rats received fullerenol nanoparticles (10 mg/kg, intraperitoneally) 30 minutes before MCA 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 (527 ± 59 mm3) in accompany with a decrease in the glutathione content (45%), and SOD activity (29%) compared with sham rats. Administration 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.