Effect of N-acetylcysteine on motor symptoms and parkin protein level in frontal cortex in rat model of Parkinson's disease

Recent studies have shown that oxidative stress has a critical role in the pathophysiology of Parkinson’s disease. Frontal cortex receives a great amount of dopaminergic neurons from nigrostriatal pathway and is one of the brain regions which aredamagedin Parkinson’s disease. On the other hand anti-oxidant properties of N-acetylcysteine have been proven to occur via fortifying glutathione. Glutathione is one of the main intracellular anti-oxidant systems. Therefore our study was aimed to evaluate the effect of N-acetylcysteine in the management of Parkinson’s disease. Male Wistar rats with age range of 10-12 months and weights of 400±50g received rotenone (2.5 mg/kg/48h ip) to induce Parkinson’s disease model. NAC (25 or 50 mg/kg/48h ip) was administered one hour before rotenone injections. In order to measure the motor symptoms and verify the development of the model, rotarod test was performed. Moreover the frontal cortex parkin level, one of the crucial proteins in Parkinson’s disease, was measured using western blot technique. The results indicated that N-acetylcysteine could prevent decline in the motor performance inrotarod test. In addition frontal cortex parkin level was significantly decreased in rotenone received animals while N-acetylcysteine prevented the reduction of parkin in this region. Our results indicated that that N-acetylcysteine could prevent the development of Parkinson’s disease in this model which is probably due to its anti-oxidant properties.