Objective: Oxidative stress plays a key role in the pathogenesis of cerebral ischemia/reperfusion (I/R) injury. In this study, we aimed to investigate the effect of N-acetylcysteine (NAC), which is known to have antioxidant properties, on oxidative stress and tissue adropin levels, in I/R-induced rat brain tissue.

Materials and Methods: The study included 24 male Wistar-Albino rats. The animals were randomly divided into 4 groups: control, Sham, I/R, and I/R+NAC. In both I/R and I/R+NAC groups, bilateral common carotid arteries were clamped for 60 min using aneurysm clips, in IR group clamps were removed and reperfusion was performed for 120 min. In the I/R+NAC group, after the removal of the clamps NAC 50 mg/kg intraperitoneally administrated in a single dose and reperfusion was performed for 120 min. At the end of the experiment, all the rats were decapitated. Serum samples were obtained and the brain tissues were removed and embedded in paraffin blocks. Sections obtained from paraffin blocks were analyzed using the avidin-biotin-peroxidase complex technique to assess adropin immunoreactivity. Serum total antioxidant status and total oxidant status levels were measured.

Results: The TAS levels and adropin immunoreactivity decreased significantly while the TOS levels increased significantly in the I/R group compared to the control group. However, the TAS levels and adropin immunoreactivity increased significantly while the TOS levels decreased significantly in the I/R+NAC group compared to the I/R group.

Conclusion: It was revealed that I/R injury decreased the adropin levels in brain tissue and adropin can provide antioxidant protection similar to NAC.