اثر شش هفته شنای تناوبی شدید بر مسیر BDNF/TrkB در موش‌های مدل پارکینسون

نوع مقاله : مقاله پژوهشی

نویسندگان

1 دانشجوی دکتری فیزیولوژی ورزشی، گروه علوم ورزشی، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.

2 دانشیار فیزیولوژی ورزشی، گروه علوم ورزشی، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.

3 دانشیار فیزیولوژی جانوری، گروه زیست‌شناسی، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.

4 استادیار فیزیولوژی ورزشی، گروه علوم ورزشی، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.

10.22080/jaep.2024.26603.2172

چکیده

اهداف: در بیماری پارکینسون، به دلیل اختلال در مسیر BDNF/TrkB، نورون‌های دوپامینرژیک دچار آسیب و مرگ می‌شوند. هدف از پژوهش حاضر بررسی اثر شش هفته شنای تناوبی شدید بر مسیر BDNF/TrkB در موش‌های پارکینسونی شده با رزرپین بود.
روش مطالعه: در این مطالعه تجربی 14 سر موش صحرایی نر بالغ از نژاد ویستار با تزریق درون صفاقی 5 میلی­گرم بر کیلوگرم وزن بدن حیوان از رزرپین، مبتلا به بیماری پارکینسون شده و به طور تصادفی در گروه‌های بیمار و تمرین قرار گرفتند. جهت بررسی اثرات القاء بیماری پارکینسون بر متغیر‌های تحقیق، 7 سر موش صحرایی سالم نیز در گروه شاهد قرار گرفتند. موش‌های صحرایی گروه تمرین طی 6 هفته به اجرای تمرین شنای تناوبی شدید (20 نوبت شنای 30 ثانیه‌ای با 30 ثانیه استراحت بین هر نوبت و 3 جلسه در هفته) پرداختند. پس از اتمام دوره تمرینی، بیان ژن BDNF و TrkB در بافت هیپوکامپ اندازه‌گیری شد. جهت تجزیه و تحلیل یافته‌های تحقیق از آزمون آنالیز واریانس یک طرفه استفاده شد.
یافته­ ها: نتایج نشان داد بیان ژن BDNF در گروه بیمار نسبت به گروه تمرین و گروه شاهد به طور معنی‌‌داری کمتر است (به ترتیب 001/0=p و 001/0=p)، اما تفاوت معنی‌داری بین گروه تمرین و شاهد مشاهده نشد. در خصوص بیان ژن TrkB نیز نتایج حاکی از کمتر بودن بیان ژن این پروتئین در گروه بیمار نسبت به گروه تمرین و گروه شاهد بود (به ترتیب 04/0=p و 03/0=p)، اما تفاوت معنی‌داری بین گروه تمرین و شاهد مشاهده نشد.
نتیجه گیری: با توجه به نتایج به دست آمده به نظر می‌رسد تمرینات شنای تناوبی شدید موجب تحریک مسیر BDNF/TrkB در بیماران پارکینسونی می‌شود. بنابراین بررسی این نوع تمرینات در بیماران پارکینسونی پیشنهاد می‌‌گردد.

کلیدواژه‌ها


عنوان مقاله [English]

The Effect of Six Weeks High Intensity Interval Swimming Training on BDNF/Trkb Pathway in Parkinson Rat Model

نویسندگان [English]

  • Mehdi Javidi 1
  • Mehrzad Moghadasi 2
  • Mohammad Amin Edalatmanesh 3
  • Mehdi Noora 4
1 Department of ٍٍ Exercise Physiology, Shiraz Branch, Islamic Azad University, Shiraz, Iran
2 Department of ٍٍ Exercise Physiology, Shiraz Branch, Islamic Azad University, Shiraz, Iran
3 Department of Biology, Shiraz Branch, Islamic Azad University, Shiraz, Iran
4 Department of Exercise Physiology, Shiraz Branch, Islamic Azad University, Shiraz, Iran
چکیده [English]

Objectives: In Parkinson's disease, due to disruption of the BDNF/TrkB pathway, dopaminergic neurons are damaged and die. The aim of present study was to examine the effect of six weeks high intensity interval swimming training on BDNF/TrkB pathway in Parkinson rat model.
Methods: In this experimental study, fourteen mature Wistar male rats were subjected to Parkinson's disease (PD) through intraperitoneally injection of 5 mg/kg reserpine and then were divided into PD group or training group randomly. Seven healthy rats were assigned to the control group. The rats in the training groups swam 20 times of 30 seconds with 30 seconds of rest between each time, 3 days a week for 6 weeks. After the 6-week intervention, BDNF and TrkB gene expressions were measured in hippocampus.
Results: Data indicated that the BDNF gene expression was lower in the PD group compare to the healthy control and training group (p=0.001 and p=0.001 respectively). No significant differences were observed between healthy control group and training group. For TrkB gene expression also data revealed that this protein gene expression was lower in the PD group compare to the healthy control and training group (p=0.04 and p=0.03 respectively), while no significant differences were observed between healthy control group and training group.
Conclusion: According to study results, it seems that high intensity interval swimming training increases brain neurotrophins content and activity in PD. Therefore, this type of exercise is recommended for future research in Parkinson's patients.

کلیدواژه‌ها [English]

  • High Intensity Interval Swimming Training
  • Parkinson's Disease
  • BDNF
  • TrkB
##Abbasi, M., Kordi, M. & Daryanoosh, F. (2023). The effect of eight weeks of high-intensity interval swimming training on the expression of PGC-1α and IL-6 proteins and memory function in brain hippocampus in rats with non-alcoholic steatohepatitis induced by high fat diet. J Appl Health Stud Sport Physiol. (In press) (In Persian). ## Abbaspoor, E., Zolfaghari, M., Ahmadi, B. & Khodaei, K. (2020). The effect of combined functional training on BDNF, IGF-1, and their association with health-related fitness in the multiple sclerosis women. Growth Horm IGF Res, 52: 101320. ## Bayati, M., Gharakhanlou, R. & Farzad, B. (2015). Adaptations of physiological performance following high-intensity interval training. Sport Physiol, 7:15-32. (In Persian) ##Bonanni, R., Cariati, I., Tarantino, U., D’Arcangelo, G. & Tancredi, V. (2022). Physical exercise and health: A focus on its protective role in neurodegenerative diseases. J Funct Morphol Kinesiol, 7: 38. ##Buhmann, C., Wrobel, N., Grashorn, W., Fruendt, O., Wesemann, K., Diedrich, S., … & Bingel, U. (2017). Pain in Parkinson disease: A cross-sectional survey of its prevalence, specifics, and therapy. J Neurology, 264: 758–769. ##Colpaert, F.C. (1987). Pharmacological characteristics of tremor, rigidity and hypokinesia induced by reserpine in rat. Neuropharmacology, 26(9): 1431-40. ##Er, S., & Airavaara, M. (2023). Protective mechanisms by glial cell line-derived neurotrophic factor and cerebral dopamine neurotrophic factor against the α-synuclein accumulation in Parkinson's disease. Biochem Soc Trans. 27; 51(1): 245-257. ##Fontanesi, C., Kvint, S., Frazzitta, G., Bera, R., Ferrazzoli, D., Di Rocco, A. … & Ghilardi M.F. (2016). Intensive rehabilitation enhances lymphocyte BDNF-TrkB signaling in patients with Parkinson's disease. Neurorehabil Neural Repair, 30: 411–8. ##Geng, X., Zou, Y., Li, J., Li, S., Qi, R., Yu, H., & Zhong L. (2023). BDNF alleviates Parkinson's disease by promoting STAT3 phosphorylation and regulating neuronal autophagy. Cell Tissue Res. 393(3): 455-470. ##Gibala, M.J., Little, J.P., MacDonald, M.J. & Hawley, J.A. (2012). Physiological adaptations to low‐volume, high‐intensity interval training in health and disease. J Physiol, 590: 1077-84. ##Goal, R. & Chaudhary, R. (2020). Effect of daidzein on Parkinson disease induced by reserpine in rats. Braz J Pharm Sci, 56: e18388. ##Hosseinzadeh, A., Baneshi, M.R., Sedighi, B., Kermanchi, J. & Haghdoost, A.K. (2021). Estimation of Parkinson's disease prevalence and its geographical variation in Iran. J Mazandaran Univ Med Sci, 31 (200): 113-124. ##Hubrecht, R, & Kirkwood, J. (2010). UFAW Handbook on the care and management of laboratory and other research animals. 8th ed. Wiley-Blackwell Publishing Ltd; 460-520. ##Jimenez-Moreno, N., & Lane, J.D. (2020). Autophagy and redox homeostasis in Parkinson’s: A crucial balancing act. Oxid Med Cell Longev, 2020: 8865611. ##Jodeiri Farshbaf, M., Ghaedi, K., Megraw, T.L., Curtiss, J., Shirani Faradonbeh, M., Vaziri, P., & Nasr-Esfahani, M.H. (2016). Does PGC1α/FNDC5/BDNF elicit the beneficial effects of exercise on neurodegenerative disorders? Neuromol Med, 18: 1–15. ##Kay, J.C., Xia, C.M., Liu, M., Shen, S., Yu, S.J., Chung, C. & Qiao, L.Y. (2013). Endogenous PI3K/Akt and NMDAR act independently in the regulation of CREB activity in lumbosacral spinal cord in cystitis. Exp Neurol, 250: 366–375. ##Lima Giacobbo, B., Doorduin, J., Klein, H.C., Dierckx, R., Bromberg, E. & de Vries, E.F.J. (2019). Brain-derived neurotrophic factor in brain disorders: Focus on neuroinflammation. Mol Neurobiol. 56: 3295–3312. ##Lu, B., Nagappan, G. & Lu, Y. (2014). BDNF and synaptic plasticity, cognitive function, and dysfunction. In neurotrophic factors. Handbook of Experimental Pharmacology; Lewin, G., Carter, B., Eds.; Springer: Berlin/Heidelberg, Germany, 223–250. ##Maass, A., Düzel, S., Brigadski, T., Goerke, M., Becke, A., Sobieray, U., … & Düzel, E. (2016). Relationships of peripheral IGF-1, VEGF and BDNF levels to exercise-related changes in memory, hippocampal perfusion and volumes in older adults. Neuroimage 2016, 131, 142–154. ##Malczynska, P., Kaminski, B., Siemiatycka, M., Pawłowska, A., Przybylska, I., Langfort, J. … & Chalimoniuk, M. High intensity interval training elevates circulating BDNF and miRNAs level in patients with idiopathic Parkinson’s disease. Mov Disord, 34 (suppl 2). ##Marsili, L., Rizzo, G. & Colosimo, C. (2018). Diagnostic criteria for Parkinson’s disease: from James Parkinson to the concept of prodromal disease. Front Neurol, 9: 156. ##McMorris, T. (2016). Developing the catecholamines hypothesis for the acute exercise-cognition interaction in humans: Lessons from animal studies. Physiol. Behav, 165: 291–299. ##Miller, K.M., Mercado, N.M. & Sortwell, C.E. (2021). Synucleinopathy-associated pathogenesis in Parkinson’s disease and the potential for brain-derived neurotrophic factor. npj Parkinson’s Disease, 7: 35. ##Nussbaum, R.L., & Ellis, C. E. (2003). Alzheimer’s disease and Parkinson’s disease. New Engl Med. 348: 1356–1364. ##O'Callaghan, A., Harvey, M., Houghton, D., Gray, W.K., Weston, K.L., Oates, L.L., … & Walker, R.W. (2020). Comparing the influence of exercise intensity on brain-derived neurotrophic factor serum levels in people with Parkinson's disease: a pilot study. Aging Clin Exp Res, 32(9): 1731-1738. ##Orefice, L.L., Waterhouse, E.G., Partridge, J.G., Lalchandani, R.R., Vicini, S. & Xu, B. (2013). Distinct roles for somatically and dendritically aynthesized brain-derived neurotrophic factor in morphogenesis of dendritic spines. J Neurosci, 33: 11618–11632. ##Palasz, E., Niewiadomski, W., Gasiorowska, A., Mietelska-Porowska, A., & Niewiadomska, G. (2019). Neuroplasticity and neuroprotective effect of treadmill training in the chronic mouse model of Parkinson’s disease. Neural Plast, 2019: 8215017. ##Palasz, E., Wysocka, A., Gasiorowska, A., Chalimoniuk, M., Niewiadomski, W. & Niewiadomska G. (2020). BDNF as a promising therapeutic agent in Parkinson’s disease. Int J Mol Sci, 21(3): 1170. ##Rangasamy, S.B., Dasarathi, S., Pahan, P., Jana, M. & Pahan, K. (2019). Low-Dose Aspirin Upregulates Tyrosine Hydroxylase and Increases Dopamine Production in Dopaminergic Neurons: Implications for Parkinson’s disease. J. Neuroimmune Pharmacol, 14: 173–187. ##Real, C.C., Ferreira, A.F.B., Chaves-Kirsten, G.P., Torrão, A.S., Pires, R.S. & Britto, L.R.G. (2013). BDNF receptor blockade hinders the beneficial effects of exercise in a rat model of Parkinson’s disease. Neuroscience, 237: 118–129.Sabaghi, A., Heirani, A., Mahmoodi, H. & Sabaghi, S. (2019). High-intensity interval training prevents cognitive-motor impairment and serum BDNF level reduction in Parkinson mice model. Sport Sci Health, 15: 681-687. ##Scalzo, P., Kümmer, A., Bretas, T.L., Cardoso, F. & Teixeira, A.L. (2010). Serum levels of brain-derived neurotrophic factor correlate with motor impairment in Parkinson’s disease. J Neurol, 257: 540–545. ##Wang, Z.H., Wu, W., Kang, S.S., Liu, X., Wu, Z., Peng, J., … & Ye, K. (2018). BDNF inhibits neurodegenerative disease-associated asparaginyl endopeptidase activity via phosphorylation by AKT. JCI Insight, 3(16): e99007. ##Wrann, C.D., White, J.P., Salogiannnis, J., Laznik-Bogoslavski, D., Wu, J., Ma, D., … & Spiegelman, B.M. (2013). Exercise Induces Hippocampal BDNF through a PGC-1α/FNDC5 Pathway. Cell Metab, 18: 649–659. ##Wu, C.H., Chen, C.C., Hung, T.H., Chuang, Y.C., Chao, M., Shyue, S.K. & Chen, S.F. (2019). Activation of TrkB/Akt signaling by a TrkB receptor agonist improves long-term histological and functional outcomes in experimental intracerebral hemorrhage. J Biomed Sci, 26: 53. ##Wu, S.Y., Wang, T.F., Yu, L., Jen, C.J., Chuang, J.I., Wu, F.S. … & Kuo, Y.M. (2011). Running exercise protects the substantia nigra dopaminergic neurons against inflammation-induced degeneration via the activation of BDNF signaling pathway. Brain Behav Immun, 25: 135–146. ##Yang, J., Luo, S., Zhang, J., Yu, T., Fu, Z., Zheng, Y., …& Zhang, Z. (2021). Exosome-mediated delivery of antisense oligonucleotides targeting alpha-synuclein ameliorates the pathology in a mouse model of Parkinson’s disease. Neurobiol Dis, 148: 105218. ##Yarrow, J.F., White, L.J., McCoy, S.C. & Borst, S.E. (2010). Training augments resistance exercise induced elevation of circulating brain derived neurotrophic factor (BDNF). Neurosci Lett, 479: 161–165. ##