Document Type : Research Paper
Authors
1
Department of Exercise Physiology, Faculty of Sport Sciences, Ferdowsi University of Mashhad.Mashhad. Iran
2
Associate Professorof Department of Exercise Physiology, Faculty of Sport Sciences, Ferdowsi University of Mashhad,, Mashhad, Iran.
3
Professor of Department of Sports Physiology, Faculty of physical education and sport sciences, Ferdowsi University of Mashhad, Mashhad, Iran
4
professor of department of exercise physiology. faculty of sport sciences. ferdowsi university of mashhad. mashhhad. iran
Abstract
Objectives: Stroke is a neurological disorder and the second leading cause of death worldwide. Recently, studies on neuroprotective treatments for stroke have become a hot topic globally. The present study aimed to investigate the neuroprotective effect of a combination of aerobic exercise and adenosine on the expression of the A2a gene and the consequences of stroke injury in the hippocampus of male rats. Materials and Methods: Fifty male Wistar rats (8-10 weeks old, weighing 240-270 grams) were randomly divided into five groups: (sham, control+ischemia, ischemia+exercise, ischemia+adenosine, and ischemia+adenosine+exercise). After inducing ischemia, rats in exercise groups performed treadmill running 5 days per week for 8 week. Adenosine simultaneously once per day to Adenosine-treated groups were injected. 48 hours after completing the exercise protocol, hippocampal tissue was collected for cell death, and measuring of the A2a expression using the RT- PCR method. The data were analyzed using Anova and post hoc Bonferroni’s test. Results: The number of dead cells increased in the ischemia group compared to the sham and decreased in the ischemia+adenosine+Exercise and ischemia+exercise groups compared to the ischemia group. The A2a expression in group ischemia+adenosine+exercise, ischemia+exercise, and ischemia+adenosine showed respectively the highest increase, with a significant difference compared to the sham (P<0/001) and control+ischemia (P<0/001) groups. Conclusion: aerobic exercise and adenosine, both independently and interactively, can serve as a neuroprotective combination by increasing the expression of the A2a and stimulating the signaling and mechanisms related to the reduction of cell death, providing therapeutic and protective effects against ischemic stroke-induced consequences.
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