| dc.description.abstract | Brain damage can cause severe cardiac complications. One of the main mechanisms involved in this process is the activation of the oxidative stress and inflammatory pathway. In this study, the molecular mediators of the inflammatory pathway of heart damage following cerebral ischemia-reperfusion in the brain in adult male rats and the protective effects of N-acetylcysteine were investigated.
Methods: In this study, 24 male Wistar rats weighing 250±20 grams were divided into 3 groups n=8. sham, IR, IR+NAC group. (Sham group, ischemia-reperfusion group, ischemia-reperfusion group + N-acetylcysteine) Ischemia was induced by clamping the bilateral common carotid artery for 20 minutes and then reperfusion for 24 hours. N-acetylcysteine with a dose of 150 mg/kg was injected intraperitoneally one hour before ischemia and 5 minutes before reperfusion. 24 hours after reperfusion, rats were anesthetized and blood and heart tissue samples were taken to measure Sirt1, eNOS, Hsp70, NF-B, CK-MB by western blot method, MDA, TAC by calorimetry method and 8-OHdG by ELISA method and hematoxin staining. - Eosin.
Results: The results of this study showed that ischemia reperfusion decreased the amount of Sirt1, eNOS and TAC compared to the sham group, but the use of NAC caused a significant increase in mentioned parameters compared to the IR group. Also, in the IR group, the amount of NF-B, 8OHdG, Hsp70, CK-MB, and MDA increased, but the use of NAC caused a significant decrease in the amount of these proteins. H&E staining also showed the positive effect of NAC in the heart. | en_US |
