Neuroprotective Effects of Fullerenol against Reperfusion Injuries after Focal Transient Cerebral Ischemia in Rat

Background and Overproduction of free radicals after brain ischemia exacerbates brain infarction and edema specifically during early reperfusion. The scavenging property of water-soluble fullerene derivatives is proven, so, the aim of this study was to evaluate the effects of fullerenol nanoparticles on brain infarction and edema, especially oxidative damages during reperfusion in an experimental model of stroke.
The experiment was performed by three groups of rats (n=24): sham, control ischemia, and ischemic treatment. Brain ischemia was induced by 90 min middle cerebral artery occlusion (MCAO) followed by 24 hours reperfusion. The rats received fullerenol (10 mg/kg IP) immediately after termination of MCAO. Neurological deficit score (NDS), infarct volume, brain edema, and brain content of malondialdehyde (MDA) were assessed 24 hours after termination of MCAO.
MCAO induced neurological dysfunction (3.20±0.20), brain infarction (527±59 mm3), and brain edema (3.83±0.53%) in control ischemic group. The content of MDA increased in ischemic brain (5.30±0.11µg/mg protein) compared with that in non-ischemic brain (0.74±0.34µg/mg protein). Administration of fullerenol in ischemic treated rats significantly reduced neurological dysfunction (2.01±0.22), brain infarction (106±33 mm3) and brain edema (1.70±0.74%). Also, fullerenol decreased the MDA content of ischemic treatment group (0.78±0.16µg/mg protein) compared with that of the control ischemic group.
Our findings indicate that fullerenol nanoparticles, as a potent antioxidant, effectively reduce reperfusion-induced brain injury and brain edema possibly through scavenging property of free radicals.