تأثیر چهار هفته شنای هوازی بر میزان عامل نورون‌زایی مشتق‌ از مغز و گیرنده‌ی آن در بافت مغز موش‌های مبتلا به انسفالومیلیت خود ایمن تجربی

نوع مقاله : مقاله های پژوهشی

نویسندگان

1 دانشجوی دکتری، گروه فیزیولوژی ورزشی، دانشکده‌ی تربیت بدنی و علوم ورزشی، دانشگاه خوارزمی، تهران، ایران

2 دانشیار، گروه فیزیولوژی ورزشی، دانشکده‌ی تربیت بدنی و علوم ورزشی، دانشگاه خوارزمی، تهران، ایران

3 استادیار، مرکز تحقیقات سلولی و مولکولی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی جندی‌شاپور اهواز، اهواز، ایران

4 استاد، گروه تربیت بدنی، دانشکده‌ی علوم انسانی، دانشگاه تربیت مدرس، تهران، ایران

5 استاد، گروه فیزیولوژی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی جندی‌شاپور اهواز، اهواز، ایران

چکیده

مقدمه: Multiple sclerosis، به عنوان یک بیماری عصبی- ایمنی‌شناسی (Neuroimmunology) در انسان شناخته می‌شود. شواهد حاکی از نقش عامل نورون‌زایی مشتق از مغز (Brain-derived neurotrophic factor یا BDNF) و گیرنده‌ی اختصاصی آن، تیروزین کیناز B (Tyrosine receptor kinase B یا TrkB) در پیشرفت این بیماری است. تأثیر عوامل مختلف بر روی بیان این عوامل در مطالعات مختلف گزارش شده است. هدف از انجام این مطالعه، تعیین تأثیر چهار هفته شنای هوازی بر میزان عوامل نورون‌زای مشتق از مغز و تیروزین کیناز B در مغز موش‌های مدل حیوانی Multiple sclerosis یا مبتلا به انسفالومیلیت خود ایمن تجربی (Experimental autoimmune encephalomyelitis یا EAE) بود.روش‌ها: موش‌های C57BL/6 به 8 گروه 10 تایی شامل 6 گروه موش‌های مدل EAE (شاهد، شنا، دریافت اینترفرون بتا-1، شنا و دریافت اینترفرون بتا-1، شاهد تزریق، شاهد شنا و تزریق) و 2 گروه موش‌های سالم (شاهد، شنا) تقسیم شدند. از روز 9 بیماری، موش‌ها به مدت 4 هفته روزانه مقدار 150 واحد بین‌المللی/گرم اینترفرون بتا-1 دریافت نمودند و یا به مدت 4 هفته، به صورت 5 روز در هر هفته و روزانه 30 دقیقه، ورزش شنا داشتند. بافت مغز جدا و سطح عوامل پیش‌گفته به روش Enzyme-linked immunosorbent assay (ELISA) سنجیده شد. داده‌ها توسط آزمون One-way ANOVA تحلیل شدند.یافته‌ها: EAE منجر به کاهش BDNF و افزایش TrkB در مغز موش‌های مدل EAE شد. همچنین، نشان داده شد که شنا و تیمار اینترفرون بتا-1، منجر به افزایش این عوامل در مغز موش‌ها شد؛ در حالی که این افزایش به صورت آماری معنی‌دار نبود.نتیجه‌گیری: بر اساس یافته‌های این مطالعه، احتمال می‌رود ورزش نسبت به داروی اینترفرون بتا-1، عامل مؤثرتری در تغییر سطح BDNF و TrkB بافت مغز موش‌های مدل EAE ‌باشد.

کلیدواژه‌ها

عنوان مقاله [English]

The Effect of Four Weeks of Aerobic Swimming on the Levels of Brain-Derived Neurotrophic Factor (BDNF) and Tyrosine Receptor Kinase B (TrkB) in the Brain of Animal Model of Experimental Autoimmune Encephalitis (EAE)

نویسندگان [English]

  • Mehdi Seyed-Alhosseini 1
  • Hamid Rajabi 2
  • Ata Allah Ghadiri 3
  • Reza Gharakhanlou 4
  • Alireza Sarkaki 5
1 PhD Student, Department of Exercise Physiology, School of Physical Education and Sports Sciences, Kharazmi University, Tehran, Iran
2 Associate Professor, Department of Exercise Physiology, School of Physical Education and Sports Sciences, Kharazmi University, Tehran, Iran
3 Associate Professor, Cellular and Molecular Research Center, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
4 Professor, Department of Physical Education, School of Humanities, Tarbiat Modares University, Tehran, Iran
5 Professor, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
چکیده [English]

Background: Multiple sclerosis (MS) is known as a neuroimmunological disease in human being. The evidences show that brain-derived neurotrophic factor (BDNF) and its specific receptor, tyrosine receptor kinase B (TrkB) play a role in the development of multiple sclerosis. Previous studies demonstrated that various interventions affect the expression of these factors. This study aimed to investigate the effect of four weeks of aerobic swimming on the level of BDNF and TrkB in the brain of mice with experimental autoimmune encephalomyelitis (EAE) or animal model of multiple sclerosis.Methods: A total number of 80 C57BL/6 mice, aging 10 to 12 weeks and weighing 20 ± 2 gram were divided into eight groups of 10, control, swimming (SW), EAE, EAE + SW, EAE + solvent (SOL), EAE + interferon-beta (IFN), EAE + environment (En) + SOL, and EAE + SW + IFN. On post-immunization day 9, animals received IFN (150 IU/g) or were subjected to swimming daily for 4 weeks (5 days/week). Brains were extracted and the levels of BDNF and TrkB were measured via enzyme-linked immunosorbent assay (ELISA). The data were analyzed using one-way ANOVA.Findings: EAE decreased BDNF and increased TrkB level in the brain of EAE-induced mice. Level of BDNF and TrkB increased in mice brain following swimming and IFN treatment; however these alterations were not significant.Conclusion: These findings suggest that probably swimming is more effective than IFN to alter the level of BDNF and TrkB in the brain of EAE-induced mice.

کلیدواژه‌ها [English]

  • Experimental autoimmune encephalomyelitis
  • Brain-derived neurotrophic factor
  • Tyrosine receptor kinase B (TrkB) receptor
  • Swimming

مراجع

  1. Compston A, Coles A. Multiple sclerosis. Lancet 2008; 372(9648): 1502-17.
  2. De SL, Annunziata P, Sessa E, Bramanti P. Brain-derived neurotrophic factor and TrkB receptor in experimental autoimmune encephalomyelitis and multiple sclerosis. J Neurol Sci 2009; 287(1-2): 17-26.
  3. Sarchielli P, Greco L, Stipa A, Floridi A, Gallai V. Brain-derived neurotrophic factor in patients with multiple sclerosis. J Neuroimmunol 2002; 132(1-2): 180-8.
  4. Constantinescu CS, Farooqi N, O'Brien K, Gran B. Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS). Br J Pharmacol 2011; 164(4): 1079-106.
  5. Ziemssen T, Kumpfel T, Klinkert WE, Neuhaus O, Hohlfeld R. Glatiramer acetate-specific T-helper 1- and 2-type cell lines produce BDNF: Implications for multiple sclerosis therapy. Brain-derived neurotrophic factor. Brain 2002; 125(Pt 11): 2381-91.
  6. Sabatier MJ, Redmon N, Schwartz G, English AW. Treadmill training promotes axon regeneration in injured peripheral nerves. Exp Neurol 2008; 211(2): 489-93.
  7. Krakowiak J, Liu C, Papudesu C, Ward PJ, Wilhelm JC, English AW. Neuronal BDNF signaling is necessary for the effects of treadmill exercise on synaptic stripping of axotomized motoneurons. Neural Plast 2015; 2015: 392591.
  8. Kim SE, Ko IG, Shin MS, Kim CJ, Jin BK, Hong HP, et al. Treadmill exercise and wheel exercise enhance expressions of neutrophic factors in the hippocampus of lipopolysaccharide-injected rats. Neurosci Lett 2013; 538: 54-9.
  9. Motl RW, Pilutti LA. The benefits of exercise training in multiple sclerosis. Nat Rev Neurol 2012; 8(9): 487-97.
  10. Andreasen AK, Stenager E, Dalgas U. The effect of exercise therapy on fatigue in multiple sclerosis. Mult Scler 2011; 17(9): 1041-54.
  11. Coelho FG, Gobbi S, Andreatto CA, Corazza DI, Pedroso RV, Santos-Galduroz RF. Physical exercise modulates peripheral levels of brain-derived neurotrophic factor (BDNF): A systematic review of experimental studies in the elderly. Arch Gerontol Geriatr 2013; 56(1): 10-5.
  12. Knaepen K, Goekint M, Heyman EM, Meeusen R. Neuroplasticity - exercise-induced response of peripheral brain-derived neurotrophic factor: A systematic review of experimental studies in human subjects. Sports Med 2010; 40(9): 765-801.
  13. Bansi J, Bloch W, Gamper U, Kesselring J. Training in MS: Influence of two different endurance training protocols (aquatic versus overland) on cytokine and neurotrophin concentrations during three week randomized controlled trial. Mult Scler 2013; 19(5): 613-21.
  14. Aharoni R, Saada R, Eilam R, Hayardeny L, Sela M, Arnon R. Oral treatment with laquinimod augments regulatory T-cells and brain-derived neurotrophic factor expression and reduces injury in the CNS of mice with experimental autoimmune encephalomyelitis. J Neuroimmunol 2012; 251(1-2): 14-24.
  15. Majidi-Zolbanin J, Doosti MH, Kosari-Nasab M, Salari AA. Prenatal maternal immune activation increases anxiety- and depressive-like behaviors in offspring with experimental autoimmune encephalomyelitis. Neuroscience 2015; 294: 69-81.
  16. Bernardes D, Brambilla R, Bracchi-Ricard V, Karmally S, Dellarole A, Carvalho-Tavares J, et al. Prior regular exercise improves clinical outcome and reduces demyelination and axonal injury in experimental autoimmune encephalomyelitis. J Neurochem 2016; 136 Suppl 1: 63-73.
  17. Chen X, Hu X, Zou Y, Pi R, Liu M, Wang T, et al. Combined treatment with minocycline and prednisone attenuates experimental autoimmune encephalomyelitis in C57 BL/6 mice. J Neuroimmunol 2009; 210(1-2): 22-9.
  18. Castellano V, White LJ. Serum brain-derived neurotrophic factor response to aerobic exercise in multiple sclerosis. J Neurol Sci 2008; 269(1-2): 85-91.
  19. Frota ER, Rodrigues DH, Donadi EA, Brum DG, Maciel DR, Teixeira AL. Increased plasma levels of brain derived neurotrophic factor (BDNF) after multiple sclerosis relapse. Neurosci Lett 2009; 460(2): 130-2.
  20. Liguori M, Fera F, Patitucci A, Manna I, Condino F, Valentino P, et al. A longitudinal observation of brain-derived neurotrophic factor mRNA levels in patients with relapsing-remitting multiple sclerosis. Brain Res 2009; 1256: 123-8.
  21. Lalive PH, Kantengwa S, Benkhoucha M, Juillard C, Chofflon M. Interferon-beta induces brain-derived neurotrophic factor in peripheral blood mononuclear cells of multiple sclerosis patients. J Neuroimmunol 2008; 197(2): 147-51.
  22. Azoulay D, Mausner-Fainberg K, Urshansky N, Fahoum F, Karni A. Interferon-beta therapy up-regulates BDNF secretion from PBMCs of MS patients through a CD40-dependent mechanism. J Neuroimmunol 2009; 211(1-2): 114-9.
  23. Caggiula M, Batocchi AP, Frisullo G, Angelucci F, Patanella AK, Sancricca C, et al. Neurotrophic factors in relapsing remitting and secondary progressive multiple sclerosis patients during interferon beta therapy. Clin Immunol 2006; 118(1): 77-82.
  24. Sarchielli P, Zaffaroni M, Floridi A, Greco L, Candeliere A, Mattioni A, et al. Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins. Mult Scler 2007; 13(3): 313-31.
  25. Neeper SA, Gomez-Pinilla F, Choi J, Cotman CW. Physical activity increases mRNA for brain-derived neurotrophic factor and nerve growth factor in rat brain. Brain Res 1996; 726(1-2): 49-56.
  26. Cotman CW, Berchtold NC. Exercise: A behavioral intervention to enhance brain health and plasticity. Trends Neurosci 2002; 25(6): 295-301.
  27. Zhu W, Acosta C, MacNeil BJ, Klonisch T, Cortes C, Doupe M, et al. Spinal cord brain derived neurotrophic factor (BDNF) responsive cells in an experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS): Implications in repair. Res Immunol 2014; 2014: 612604.
  28. Khan N, Gordon R, Woodruff TM, Smith MT. Antiallodynic effects of alpha lipoic acid in an optimized RR-EAE mouse model of MS-neuropathic pain are accompanied by attenuation of upregulated BDNF-TrkB-ERK signaling in the dorsal horn of the spinal cord. Pharmacol Res Perspect 2015; 3(3): e00137.
  29. Kim YM, Ji ES, Kim SH, Kim TW, Ko IG, Jin JJ, et al. Treadmill exercise improves short-term memory by enhancing hippocampal cell proliferation in quinolinic acid-induced Huntington's disease rats. J Exerc Rehabil 2015; 11(1): 5-11.
  30. Badowska-Szalewska E, Spodnik E, Klejbor I, Morys J. Effects of chronic forced swim stress on hippocampal brain-derived neutrophic factor (BDNF) and its receptor (TrkB) immunoreactive cells in juvenile and aged rats. Acta Neurobiol Exp (Wars) 2010; 70(4): 370-81.
  31. Skup M, Dwornik A, Macias M, Sulejczak D, Wiater M, Czarkowska-Bauch J. Long-term locomotor training up-regulates TrkB(FL) receptor-like proteins, brain-derived neurotrophic factor, and neurotrophin 4 with different topographies of expression in oligodendroglia and neurons in the spinal cord. Exp Neurol 2002; 176(2): 289-307.
  32. Macias M, Dwornik A, Skup M, Czarkowska-Bauch J. Confocal visualization of the effect of short-term locomotor exercise on BDNF and TrkB distribution in the lumbar spinal cord of the rat: the enhancement of BDNF in dendrites? Acta Neurobiol Exp (Wars) 2005; 65(2): 177-82.
  33. Gomez-Pinilla F, Ying Z, Roy RR, Molteni R, Edgerton VR. Voluntary exercise induces a BDNF-mediated mechanism that promotes neuroplasticity. J Neurophysiol 2002; 88(5): 2187-95.
مجله دانشکده پزشکی اصفهان
دوره 35، شماره 448 - شماره پیاپی 448
مهر و آبان 1396
صفحه 1263-1270

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سابقه مقاله

  • تاریخ دریافت: 23 مرداد 1396
  • تاریخ بازنگری: 06 اردیبهشت 1403
  • تاریخ پذیرش: 17 فروردین 1401

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