Document Type : Original Article (s)
                            
                        
                                                    Authors
                            
                                                            
                                                                            1
                                                                        Assistant Professor, Department of Anatomy, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran                                
                                                            
                                                                            2
                                                                        Associate Professor, Cellular and Molecular Research Center AND Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran                                
                                                            
                                                                            3
                                                                        Assistant Professor, Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran                                
                                                            
                                                                            4
                                                                        Associate Professor, Department of Anatomy, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran                                
                            
                                                
                        
                            Abstract
                            Background: In brain ischemia, blood and oxygen supply decrease and after reperfusion, free radicals and reactive oxygen species (ROS) cause severe damage. As hippocampal injury after ischemia-reperfusion causes some complications, in this study we analyzed the effect of adenosine receptor agonist (N6-cyclopentyladenosine or CPA) and ascorbic acid on ultrastructure of hippocampal CA1 neurons after ischemia-reperfusion.Methods: 35 male rats in 5 groups were used. Ischemia-reperfusion performed by occlusion of common carotids for 15 minutes. CPA and ascorbic acids were intraperitoneally injected for 7 days after ischemia, and 2 weeks before and for 7 days after ischemia, respectively. After 20 days, brain samples were isolated, prepared, and assayed using transmission electron microscopy (TEM).Findings: Ultrastructure assay of hippocampal CA1 neurons after ischemia-reperfusion with transmission electron microscopy showed recovery of intracellular organelles particularly mitochondria of treated groups. In combination therapy, these improvements were better.Conclusion: Intraperitoneal injection of CPA and ascorbic acid after ischemia-reperfusion can reduce neural damage in CA1 region of hippocampus.
                        
                        
                        
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