Abstract:
Grape Seed Extracts (GSE) contain a number of polyphenols including proanthocyanidins and procyanidins, powerful free radical scavengers, are intended for use in food as functional ingredients exhibiting antioxidant activity. It is extracted from grape seed waste product obtained from grape fruit (Vitis vernifera, Linn). GSE have been reported to possess a broad spectrum of pharmacological and therapeutic effects including neuroprotective effect. The purpose of the present study was to investigate neuroprotective effect of grape seed extract on oxidative stress and brain damage induced by high-fat diet in rats. Forty rats were randomly divided into 5 groups. Each group comprised of 8 rats. These extracts were incorporated into chow and fed to rats for 8 weeks (60 days). Group I were fed normal diets (normal group), group II were fed high-fat diets (high-fat diet group), group III were fed high-fat diets and were orally administered with fenofibrate 100 mg/kg/day at 4th weeks (reference group). Groups IV and V were fed high-fat diets containing GSE at the concentrations of 0.5% and 1.0%, respectively. At the end of the experiment, all rats were anesthesized with pentobarbital (60 mg/kg). Blood was collected from left ventricle and their brain were immediately removed dissected for cerebral cortex, cerebellum and hippocampus for pathological investigation of neuronal death (dark neuron counting). Brain homogenates was prepared for investigation of nitric oxide (NO) production and lipid peroxidation. Lipid peroxidation (malondialdehyde, MDA) in brain tissue and blood were examied. The results showed that GSE decreased MDA and NO production levels in brain tissue. Increasing of NO production and decreasing of MDA level in blood were found compairing with high-fat diet group. Furthermore, histopathologically examination showed that GSE prevented the high-fat diets induced cellular injury in brain tissue. These findings demonstrated that GSE potentially possess a benefit on neuroprotective effect from high-fat diets induced neuronal death via its lipid lowering effect and antioxidant activity