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mljgoums 2019, 13(6): 23-28 |
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Yazdanian M, Moazami M, Shabani M, Cheragh Birjandi S. Effects of Exercise Preconditioning on Neurotrophin-4 and Tropomyosin Receptor Kinase B Expression in the Hippocampal CA1 Region Following Transient Global Cerebral Ischemia/Reperfusion in Wistar Rats. mljgoums 2019; 13 (6) :23-28
URL: http://mlj.goums.ac.ir/article-1-1191-en.html
URL: http://mlj.goums.ac.ir/article-1-1191-en.html
1- Department of Physical Education and Sport Sciences, Islamic Azad University, Bojnourd Branch, Bojnord , Iran
2- Associate Professor in Sport Physiology, Faculty of Sport Sciences, Ferdowsi University of Mashhad, Mashhad, Iran. ,mahtab.moazami@gmail.com
3- Associate Professor, Department of Sport Sciences, University of Bojnord, Bojnord, Iran
4- Assistant Professor, Department of Sport Science, Islamic Azad University, Bojnourd Branch, Bojnourd, Iran.
2- Associate Professor in Sport Physiology, Faculty of Sport Sciences, Ferdowsi University of Mashhad, Mashhad, Iran. ,
3- Associate Professor, Department of Sport Sciences, University of Bojnord, Bojnord, Iran
4- Assistant Professor, Department of Sport Science, Islamic Azad University, Bojnourd Branch, Bojnourd, Iran.
Abstract: (7951 Views)
ABSTRACT
Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.
Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.
ABSTRACT
Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.
Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.
Research Article: Original Paper |
Subject:
Sport Physiology
Received: 2019/02/7 | Accepted: 2019/04/6 | Published: 2019/10/30 | ePublished: 2019/10/30
Received: 2019/02/7 | Accepted: 2019/04/6 | Published: 2019/10/30 | ePublished: 2019/10/30
References
1. Duncan PW, Sullivan KJ, Behrman AL, Azen SP, Wu SS, Nadeau SE, et al. Body-weight-supported treadmill rehabilitation after a stroke. New England Journal of Medicine. 2011; 364 (21): 2026-2036. [DOI:10.1056/NEJMoa1010790]
2. Stranahan AM, Zhou Y, Martin B, Maudsley S. Pharmacomimetics of exercise: novel approaches for hippocampally-targeted neuroprotective agents. Curr Med Chem. 2009; 16(35): 4668-78. [DOI:10.2174/092986709789878292]
3. Deister C, Schmidt CE. Optimizing neurotrophic factor combinations for neurite outgrowth. J Neural Eng. 2006; 3(2): 172-9. [DOI:10.1088/1741-2560/3/2/011]
4. Persson H, Ibáñez CF. Role and expression of neurotrophins and the trk family of tyrosine kinase receptors in neural growth and rescue after injury. Curr Opin Neurol Neurosurg. 1993; 6(1): 11-8.
5. Chan KM, Lam DT, Pong K, Widmer HR, Hefti F. Neurotrophin-4/5 treatment reduces infarct size in rats with middle cerebral artery occlusion. Neurochemical Research. 1996; 21(7): 763-767. [DOI:10.1007/BF02532298]
6. Liebelt B, Papapetrou P, Ali A, Guo M, Ji X, Peng C, et al. Exercise preconditioning reduces neuronal apoptosis in stroke by up-regulating heat shock protein-70 (thermal shock protein-72) and extracellular-signal-regulated kinase 1/2. Neuroscience. 2010; 166(4): 1091-1100. [DOI:10.1016/j.neuroscience.2009.12.067]
7. Zwagerman N, Plumlee C, Guthikonda M, Ding Y. Toll-like receptor-4 and cytokine cascade in stroke after exercise. Neurological research. 2010; 32(2): 123-126. [DOI:10.1179/016164109X12464612122812]
8. Kochanski R, Dornbos D, Ding Y. Neuroprotection and Physical Preconditioning: Exercise, Hypothermia, and Hyperthermia, in Innate Tolerance in CNS. Springer. 2013; 105-131. [DOI:10.1007/978-1-4419-9695-4_5]
9. Dornbos D, Ding Y. Mechanism of Neuroprotection Underlying Physical Exercise in Ischemia-Reperfusion Injury, in Brain Injury-Pathogenesis, Monitoring, Recovery and Management. InTech. 2012; DOI: 10.5772/32119. [DOI:10.5772/32119]
10. Erfani S, Khaksari M, Oryan S, Shamsaei N, Aboutaleb N, Nikbakht F. Nampt / PBEF / visfatin exerts neuroprotective effects against ischemia / reperfusion injury by modulating the Bax / Bcl-2 ratio and preventing caspase-3 activation. J Mol Neurosci. 2015; 56(1): 237-43. doi: 10.1007/s12031-014-0486-1. [DOI:10.1007/s12031-014-0486-1]
11. Bang OY. Multimodal MRI for ischemic stroke: from acute therapy to preventive strategies. J Clin Neurol. 2009; 5(3): 107-119.doi: 10.3988/jcn.2009.5.3.107. [DOI:10.3988/jcn.2009.5.3.107]
12. Jia J, Hu YS, Wu Y, Yu HX, Liu G, Zhu DN, et al. Treadmill pre-training suppresses the release of glutamate resulting from cerebral ischemia in the rat. Exp Brain Res. 2010; 204(2): 173-9. [DOI:10.1007/s00221-010-2320-5]
13. Moskowitz MA, Lo EH, Iadecola C. The science of stroke: mechanisms in the search of treatments. Neuron. 2010; 67(2): 181-98. doi: 10.1016/j.neuron.2010.07.002. [DOI:10.1016/j.neuron.2010.07.002]
14. Sairanen TR, Lindsberg PJ, Brenner M, Carpén O, Sirén A. Differential cellular expression of tumor necrosis factor-alpha and Type I tumor necrosis factor receptor after transient global forebrain ischemia. J Neurol Sci. 2001; 186(1-2): 87-99. [DOI:10.1016/S0022-510X(01)00508-1]
15. Jia J, Hu YS, Wu Y, Liu G, Yu HX, Zheng QP, et al. Pre-ischemic treadmill training affects glutamate and gamma aminobutyric acid levels in the striatal dialysis of a rat model of cerebral ischemia. Life sciences. 2009; 84(15-16): 505-511. [DOI:10.1016/j.lfs.2009.01.015]
16. Wang X, Zhang M, Feng R, Li2, Ren W, Zhang F. Exercise Preconditioning, alleviating brain damage through excitatory amino acid transporter 2 and extracellular signalregulated kinase 1/2 after ischemic stroke in the rat. Mol Med Rep. 2015; 11(2): 1523-7 [DOI:10.3892/mmr.2014.2834]
17. Kuipers SD, Bramham CR. Brain-derived neurotrophic factor mechanisms and function in adult synaptic plasticity: new insights and implications for therapy. Curr Opin Drug Discov Devel. 2006; 9(5): 580-6.
18. Ding YH, Luan XD, Li J, Rafols JA, Guthinkonda M, Diaz FG, et al. Exercise-induced overexpression of angiogenic factors and reduction of ischemia / reperfusion injury in stroke. Current neurovascular research, 2004; 1(5): 411-420. [DOI:10.2174/1567202043361875]
19. Schäbitz W, Steigleder T, Cooper-Kuhn CM, Schwab S, Sommer C, et al. The intravenous brain-derived neurotrophic factor enhances post-trauma sensorimotor recovery and stimulates neurogenesis. Stroke. 2007; 38(7): 2165-2172. [DOI:10.1161/STROKEAHA.106.477331]
20. Oyesiku NM1, Evans CO, Houston S, Darrell RS, Smith JS, Fulop ZL, et al. Regional changes in the expression of neurotrophic factors and their receptors following acute traumatic brain injury in the adult rat brain. Brain Research. 1999; 833(2): 161-172. [DOI:10.1016/S0006-8993(99)01501-2]
21. Leasure JL, Jones M. Forced and voluntary exercise differentially affect brain and behavior. Neuroscience. 2008; 156(3): 456-65. doi: 10.1016/j.neuroscience.2008.07.041. [DOI:10.1016/j.neuroscience.2008.07.041]
22. Brown DA, Johnson MS, Armstrong CJ, Lynch JM, Caruso NM, Ehlers LB, et al. Short-term treadmill running in the rat: what kind of stressor is it? J Appl Physiol(1985). 2007; 103(6): 1979-85. [DOI:10.1152/japplphysiol.00706.2007]
23. Svensson M, Rosval P, Boza-Serrano A, Andersson E, Lexel J, Deierborg T. Forced treadmill exercise can induce stress and increase neuronal damage in a mouse model of global cerebral ischemia. Neurobiology of stress. 2016; 5: 8-18. [DOI:10.1016/j.ynstr.2016.09.002]
24. McEwen BS. Stress and Hippocampal Plasticity. Anna Rev Neurosci. 1999; 22: 105-22. [DOI:10.1146/annurev.neuro.22.1.105]
25. Li XX, Nomura T, Aihara H, Nishizaki T. Adenosine enhances glial glutamate efflux via A2a adenosine receptors. Life sciences. 2001; 68(12): 1343-1350. [DOI:10.1016/S0024-3205(00)01036-5]
26. Williams-Karnesky RL, Stenzel-Poore MP. Adenosine and Stroke: maximizing the therapeutic potential of adenosine as a prophylactic and acute neuroprotectant. Curr Neuropharmacol. 2009; 7(3): 217-27. doi: 10.2174/157015909789152209. [DOI:10.2174/157015909789152209]
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