TY - JOUR T1 - Effects of Atorvastatin on Hippocampal CA1 Cells Following Transient Global Ischemia in Male Rats TT - اثر آتورواستاتین بر سلول‌های هرمی ناحیه CA1 هیپوکامپ رت نر به دنبال ایسکمی- ریپرفیوژن JF - gums-med JO - gums-med VL - 24 IS - 93 UR - http://journal.gums.ac.ir/article-1-941-en.html Y1 - 2015 SP - 39 EP - 46 KW - Apoptosis KW - Atorvastatin KW - Hippocampus KW - Ischemia KW - Reperfusion N2 - Abstract Introduction: Ischemic stroke is a major cause of death in the world after cancer and heart attack. CA1 hippocampus is one of the most sensitive parts of the brain to ischemia and hypoxia. Antioxidants prevent cell damage consequent cell death by omitting free radicals and component resulted from cell damage. Objective: Evaluating the protective effect of atorvastatin on hippocampal CA1 cells following transient global ischemia in male rats Materials and Methods: This experimental study was conducted on a total of 24 male adult NMRI rats weighing 250-300 g with average age of 8-10 weeks. They were randomly divided into four groups: control, sham, vehicle and treatment. To produce ischemia reperfusion model, common carotid artery in both sides were blocked for 20 minutes. First dose atorvastatin (10 mg/kg) in the treatment group was administrated after 6 hours following ischemia reperfusion, then 24, 48 and 72 hours intraperitoneal. After four days, all rats were killed, and the brain were dissected and processed for nissl histological staining. The results were analyzed by analysis of variance (ANOVA) and Tukey’s tests. Results: In the present study, there was no significant difference in the number of pyramidal cell in CA1hippocampus between the treatment group and control group. But the number of healthy pyramidal cells in ischemia and vehicle groups decreased, and there was a statistically significant difference between them and control group (P<0.05). Conclusion: Present findings suggest that using atorvastatin 10mg/kg after transient ischemia reperfusion, can decrease severity of damage and cell death in CA1hippocampus cells. M3 ER -