Effect of N-acetyl cysteine on alpha- synuclein expression, its downstream target genes and apoptosis in the cerebral cortex of adult male rat models of ischemia-reperfusion

Abstract

Stroke is one of the most common causes of death and disability in adults. Since reperfusion, as the mainstay of treatment following ischemia aggravates tissue damage, this study was designed and performed to investigate the effect of N-acetylcysteine treatment on the expression of α-synuclein, 3-nitrotyrosine, PLK2, phospho-Drp1, and cleaved caspase-3 in the cerebral cortex of ischemia-reperfusion model of adult male rats. Methods: 24 rats were randomly divided into 3 groups: 1) sham group, 2) ischemia-reperfusion (IR) group and 3) ischemia-reperfusion group + N-acetylcysteine (IR+NAC). To induce global brain ischemia, under anesthesia, the common carotid artery was occluded for 20 minutes, and then reperfused. NAC in 150 mg/kg was injected intraperitoneally one hour before ischemia and also 5 minutes before the start of reperfusion. 24 hours after reperfusion, the brain tissue was removed following the protocols and the cortex tissue was isolated. The right cortex was frozen at -80°C to measure the expression of proteins by western blot method. Results: Induction of ischemia-reperfusion increased the expression of α-synuclein protein in the brain cortex of rats, which was associated with the enhanced expression of PLK2, 3-nitrotyrosine, phospho-Drp1, and cleaved caspase-3 proteins. The key finding of this study was that the injection of N-acetylcysteine improved ischemia-reperfusion injury and decreased the expression of these proteins in the brain cortex of ischemia-reperfusion model rats.