اثر تمرین مقاومتی همراه با ویتامینD با پوشش کیتوزان بر بیان ژن هایSemaphorine-a3 وNLRP-1 پیوستگاه عصبی عضله چهار سر ران رت های یائسه

نوع مقاله : مقاله پژوهشی

نویسندگان

1 گروه فیزیولوژی ورزشی، واحد تهران مرکزی، دانشگاه آزاد اسلامی، تهران، ایران

2 گروه فیزیولوژی ورزشی، واحد مهاباد، دانشگاه آزاد اسلامی، مهاباد، ایران

3 گروه تربیت‌بدنی، واحد پردیس، دانشگاه آزاد اسلامی، پردیس، ایران

چکیده

زمینه و هدف: فرآیند یائسگی باعث انحطاط نورون‌های عصب حرکتی تارهای تند انقباض می‌شود. اما اثر تمرین مقاومتی همراه با مکمل ویتامینD ترکیبی بر مهار ژن‌های موثر درآتروفی به خوبی مشخص نیست. بر این اساس هدف از مطالعه حاضر بررسی اثر 8 هفته تمرین مقاومتی همراه با ویتامینD با پوشش کیتوزان بر بیان ژن‌های Semaphorine-a3 وNLRP-1 پیوستگاه عصبی عضله چهار سر ران رتهای یائسه بود.
روش بررسی: در یک کارآزمایی پیش بالینی، 42 سر موش صحرائی ماده نژاد ویستار 8 تا 12 هفته‌ای، با میانگین وزن 230 تا 260 گرم، به طور تصادفی به 6 گروه 7 تایی: کنترل سالم (NC)، کنترل یائسه (OC)، استروژن (E)، تمرین مقاومتی (RT)، ویتامینD با کیتوزان(Vit D+Ca+2)، تمرین مقاومتی+ ویتامینD با کیتوزان(Ca+2+RT+Vit D) تقسیم شدند. پس از اوارکتومی، گروه تمرین مقاومتی 5 روز در هفته به مدت 8 هفته تمرین خود را انجام دادند. ویتامین D با کیتوزان در دوز 100 میلی‌گرم بر کیلوگرم قبل از تمرین گاواژ شد. جهت تعیین بیان ژن‌های Semaphorin-a3 و NLRP-1 خارج شد.
یافته‌ها: بیان ژنSemaphorine-a3 در گروه تمرین مقاومتی+ ویتامینD با کیتوزان نسبت به گروه کنترل یائسه(001/0P=) و گروه تمرین (002/0P=)کاهش معناداری داشت. بیان ژن NLRP-1 در گروه تمرین مقاومتی+ ویتامینD با کیتوزان نسبت به گروه تمرین کاهش معناداری داشت (043/0P=).
نتیجه‌گیری: تمرین مقاومتی باعث کاهش بیان ژن‌هایSemaphorine-a3 وNLRP-1 شد و ویتامینD با پوشش کیتوزان اثر تمرین مقاومتی را بر کاهش بیان ژن NLRP-1 افزایش داده و احتمالا می‌تواند عملکرد عصبی- عضلانی را در افراد یائسه بهبود دهد.

کلیدواژه‌ها


عنوان مقاله [English]

Effect of resistance training and vitamin D with chitosan coating on Semaphorine-a3 and NLRP-1 genes of neural junction in quadriceps muscle of ovariectomized rats

نویسندگان [English]

  • Tahereh Shadpour Alizadeh 1
  • Mohammad Ali Azarbayjani 1
  • Sirvan Atashak 2
  • Maghsoud Peeri 1
  • Saleh Rahmati Ahmad Abad 3
1 Department of Exercise Physiology , Central Tehran Branch, Islamic Azad University, Tehran, Iran
2 Department of Exercise Physiology , Mahabad Branch, Islamic Azad University, Mahabad, Iran
3 Department of Physical Education, Pardis Branch, Islamic Azad University, Pardis, Iran
چکیده [English]

Background and Objective: The menopausal process causes degeneration of motor nerve neurons in fast-twitch fibers. However, the effect of resistance training with vitamin D supplementation on the inhibition of genes involved in atrophy is not well understood. The purpose of this study was to determine the effect of resistance training and vitamin D with chitosan coating on Semaphorine-a3 and NLRP-1genes of neural junction in quadriceps muscle of postmenopausal rats.
Materials and Methods: In this experimental study, 42 femal of wistare rats with ages 8 to 12 weeks with an average weight of 230 to 260 g were randomly divided into 6 groups of 7 numbers; normal control (NC), menopause control (OC), estrogen (E), resistance training (RT),vitamin D white chitosan (Vit D+Ca+2), resistance training+Vitamin D with chitosan (RT+Vit D+Ca+2). Training group performed resistance training five days a week for eight weeks. Vitamin D with chitosan was gavage at a dose of 100 mg/kg before exercise. PCR Real time was used to determine the expression of Semaphorine-a3 and NLRP-1genes.
Results: The gene of Semaphorine-a3 in the resistance training group+vitamin D with chitosan compared to the postmenopausal control group and the training group had a significant decrease (P=0.001) and (P=0.002), respectively.  NLRP-1 gene in the resistance training group+vitamin D with chitosan was significantly reduced compared to the training group (P=0.043).
Conclusion: The results showed that resistance training decreased the  genes expression of Semaphorine-a3 and NLRP-1. Decreased expression of NLRP-1 gene under the influence of resistance training combined with vitamin D with chitosan coating could possibly improve neuromuscular function in postmenopausal people.

کلیدواژه‌ها [English]

  • Resistance training
  • Vitamin D with chitosan
  • Menopause
  • Semaphorine-a3
  • NLRP-1
  1. Douchi T, Iemura A, Matsuo T, Kuwahata T, Oki T, Yoshimitsu N, et al. Relationship of head lean mass to regional bone mineral density in elderly postmenopausal women. Maturitas 2003;46(3):225-30.
  2. Rosado MdL, Tomás MT, Correia SC, Gonçalves CR, Abreu MHd, Cardoso SF. Resistance training for muscle strength and lean mass in adults older than 60 years: a systematic review. Indian Journal of Medical Research and Pharmaceutical Sciences 2016;3(9):16-27.
  3. Saravia F, Beauquis J, Pietranera L, De Nicola AF. Neuroprotective effects of estradiol in hippocampal neurons and glia of middle age mice. Psychoneuroendocrinology 2007;32(5):480-92.
  4. Bolland MJ, Grey A, Gamble GD, Reid IR. Calcium and vitamin D supplements and health outcomes: a reanalysis of the Women’s Health Initiative (WHI) limited-access data set. The American Journal of Clinical Nutrition 2011;94(4):1144-9.
  5. Kupr B, Schnyder S, Handschin C. Role of nuclear receptors in exercise-induced muscle adaptations. Cold Spring Harbor Perspectives in Medicine 2017;7(6):a029835.
  6. Airaksinen MS, Eilers J, Garaschuk O, Thoenen H, Konnerth A, Meyer M. Ataxia and altered dendritic calcium signaling in mice carrying a targeted null mutation of the calbindin D28k gene. Proceedings of the National Academy of Sciences 1997;94(4):1488-93.
  7. Rowan SL, Rygiel K, Purves-Smith FM, Solbak NM, Turnbull DM, Hepple RT. Denervation causes fiber atrophy and myosin heavy chain co-expression in senescent skeletal muscle. PloS One 2012;7(1):e29082.
  8. Deschenes MR, Roby MA, Eason MK, Harris MB. Remodeling of the neuromuscular junction precedes sarcopenia related alterations in myofibers. Experimental Gerontology 2010;45(5):389-93.
  9. De Winter F, Vo T, Stam FJ, Wisman LA, Bär PR, Niclou SP, et al. The expression of the chemorepellent Semaphorin 3A is selectively induced in terminal Schwann cells of a subset of neuromuscular synapses that display limited anatomical plasticity and enhanced vulnerability in motor neuron disease. Molecular and Cellular Neuroscience 2006;32(1-2):102-17.
  10. Svensson A, Libelius R, Tågerud S. Semaphorin 6C expression in innervated and denervated skeletal muscle. Journal of Molecular Histology 2008;39(1):5-13.
  11. Vo TT. Studies on semaphorin 3A in the neuromuscular junction and in perineuronal nets: Vrije Universiteit 2011.
  12. Karakelides H, Nair KS. Sarcopenia of aging and its metabolic impact. Current Topics in Developmental Biology 2005;68:123-48.
  13. Martinon F, Burns K, Tschopp J. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-β. Molecular Cell 2002;10(2):417-26.
  14. de Rivero Vaccari JP, Dietrich WD, Keane RW. Activation and regulation of cellular inflammasomes: gaps in our knowledge for central nervous system injury. Journal of Cerebral Blood Flow & Metabolism 2014;34(3):369-75.
  15. Uchitel O, Protti D, Sanchez V, Cherksey B, Sugimori M, Llinas R. P-type voltage-dependent calcium channel mediates presynaptic calcium influx and transmitter release in mammalian synapses. Proceedings of the National Academy of Sciences 1992;89(8):3330-3.
  16. Jubeau M, Zory R, Gondin J, Martin A, Maffiuletti NA. Late neural adaptations to electrostimulation resistance training of the plantar flexor muscles. European Journal of Applied Physiology 2006;98(2):202-11.
  17. Little JP, Safdar A, Bishop D, Tarnopolsky MA, Gibala MJ. An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 2011;300(6)R1303-10.
  18. Gharakhanlou R, Chadan S, Gardiner P. Increased activity in the form of endurance trainig increases calcitonin gene-related peptide content in lumbar motoneuron cell bodies in the rat. Neuroscience 1999;89(4):1229-39.
  19. Glouzon BJ, Barsalani R, Lagacé J, Dionne I. Muscle mass and insulin sensitivity in postmenopausal women after 6-month exercise training. Climacteric 2015;18(6):846-51.
  20. Gharakhanlou R, Chadan S, Gardiner P. Increased activity in the form of endurance training increases calcitonin gene-related peptide content in lumbar motoneuron cell bodies and in sciatic nerve in the rat. Neuroscience 1999;89(4):1229-39.
  21. Maffiuletti NA, Zory R, Miotti D, Pellegrino MA, Jubeau M, Bottinelli R. Neuromuscular adaptations to electrostimulation resistance training. American Journal of Physical Medicine & Rehabilitation 2006;85(2):167-75.
  22. Silva Neto LS, Karnikowiski MG, Tavares AB, Lima RM. Associação entre sarcopenia, obesidade sarcopênica e força muscular com variáveis relacionadas de qualidade de vida em idosas. Brazilian Journal of Physical Therapy 2012;16:360-7.
  23. Bautista-Baños S, Hernandez-Lauzardo AN, Velazquez-Del Valle MG, Hernández-López M, Barka EA, Bosquez-Molina E, et al. Chitosan as a potential natural compound to control pre and postharvest diseases of horticultural commodities. Crop Protection 2006;25(2):108-18.
  24. Chen C, Noland KA, Kalu DN. Modulation of intestinal vitamin D receptor by ovariectomy, estrogen and growth hormone. Mechanisms of Ageing and Development 1997;99(2):109-22.
  25. Prestes J, Leite R, Pereira G, Shiguemoto G, Bernardes C, Asano R, et al. Resistance training and glycogen content in ovariectomized rats. International Journal of Sports Medicine 2012;33(07):550-4.
  26. Shetta A, Kegere J, Mamdouh W. Comparative study of encapsulated peppermint and green tea essential oils in chitosan nanoparticles: Encapsulation, thermal stability, in-vitro release, antioxidant and antibacterial activities. International Journal of Biological Macromolecules 2019;126:731-42.
  27. Kraemer WJ, Ratamess NA, French DN. Resistance training for health and performance. Current Sports Medicine Reports 2002;1(3):165-71.
  28. Mejías-Peña Y, Rodriguez-Miguelez P, Fernandez-Gonzalo R, Martínez-Flórez S, Almar M, de Paz JA, et al. Effects of aerobic training on markers of autophagy in the elderly. Age 2016;38(2):1-12.
  29. Beauchamp EM, Platanias LC. The evolution of the TOR pathway and its role in cancer. Oncogene 2013;32(34):3923-32.
  30. Lenhare L, Crisol BM, Silva VR, Katashima CK, Cordeiro AV, Pereira KD, et al. Physical exercise increases Sestrin 2 protein levels and induces autophagy in the skeletal muscle of old mice. Experimental Gerontology 2017;97:17-21.
  31. Forbes SC, Little JP, Candow DG. Exercise and nutritional interventions for improving aging muscle health. Endocrine 2012;42(1):29-38.
  32. Gyorkos AM, Spitsbergen JM. GDNF content and NMJ morphology are altered in recruited muscles following high‐speed and resistance wheel training. Physiological Reports 2014;2(2):e00235.
  33. Li Y-P, Chen Y, John J, Moylan J, Jin B, Mann DL, et al. TNF‐α acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle. The FASEB Journal 2005;19(3):362-70.
  34. Schiffer T, Geisler S, Sperlich B, Strüder H. MSTN mRNA after varying exercise modalities in humans. International Journal of Sports Medicine 2011;32(09):683-7.
  35. Mahdavian S, Ghazalian F, ebrahim k, Abed Natanzi H. The Effect of Resistance Training and Vitamin D Supplementation on Fibroblast Growth Factor 23 and Klotho Protein in Male Rats with Renal Failure. The Scientific Journal of Rehabilitation Medicine 2022.116428.2925.
  36. Abbas Saremi, Nader Shavandi, Hajar Vafapour. Eight-week resistance training with vitamin D supplementation in postmenopausal women: Effects on skeletal muscle. Pajoohande 2013;18(2):57-63.
  37. Gyorkos AM, McCullough MJ, Spitsbergen JM. Glial cell line-derived neurotrophic factor (GDNF) expression and NMJ plasticity in skeletal muscle following endurance exercise. Neuroscience 2014;257:111-8.
  38. Ercan E, Han JM, Di Nardo A, Winden K, Han MJ, Hoyo L, et al. Neuronal CTGF/CCN2 negatively regulates myelination in a mouse model of tuberous sclerosis complex. Journal of Experimental Medicine 2017;214(3):681-697.