The Effect of pre-conditioning Endurance Training on Neurogenic and Anti-Neurogenic Factor in Hippocampus of Male Rats Following Ischemic reperfusion
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Paper ID : 1921-12THCONG
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1گروه تربیت بدنی و علوم ورزشی، دانشکده علوم انسانی، دانشگاه آزاد اسلامی واحد بجنورد
22. Associate Professor, Department of Exercise Physiology, Faculty of Sport Sciences, University of Mazandaran, Babolsar, Iran
3گروه تربیت بدنی و علوم ورزشی، دانشگاه آزاد اسلامی واحد بجنورد
Introduction: binding of brain derived neurotrophic factor (BDNF) to tyrosine kinase B (TrkB) receptor leads to cell survival, while proBDNF binding to p75 receptor leads to cell death. Thus the aim of present study was to investigate the effects of eight weeks pre-conditioning endurance training on levels of BDNF, TrkB, proBDNF and p75 levels in the hippocampus male rats following ischemic reperfusion.
Materials and methods: 40 male wistar rats were divided into four groups, including: ischemic control, ischemic training, healthy control, healthy training. Training groups (healthy and ischemic), trained with 30m/min (70% VO2max), 30min/day, and 5 days/week on the treadmill. To induce ischemia, carotid artery is clamped with microsurgery clamp for 45 minutes. For data analysis, one-way ANOVA and post hoc Tukey tests were performed.
Results: BDNF levels in hippocampus of ischemic control group were significantly lower than healthy control group (p=0.001). Also BDNF levels in hippocampus of ischemic training group were higher than ischemic control group (p=0.002). Despite increasing in TrkB levels of ischemic training group than ischemic control group wasn’t significant (P=0.556). proBDNF levels in ischemic control group were significantly higher than healthy control group (P=0.001). No significant difference were found in p75 levels in difference were found in different group (p=0.071).
Conclusion: Based on these results, it seems that pre conditioning endurance training can have neuroprotective effect through improving BDNF, TrkB and proBDNF levels in hippocampus and can prevent apoptosis and neuronal death following ischemic reperfusion and can be studied as a complementary therapy in ischemic disease.