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تاثیر لیگاسیون عصب نخاعی بر بیان ژنهای Tweakو Fn14 عضله EDL موشهای نر ویستار پس از یک دوره تمرین HIT | ||
پژوهشنامه فیزیولوژی ورزشی کاربردی | ||
مقاله 10، دوره 15، شماره 30، دی 1398، صفحه 161-174 اصل مقاله (864.36 K) | ||
نوع مقاله: مقاله پژوهشی | ||
شناسه دیجیتال (DOI): 10.22080/jaep.2019.15644.1848 | ||
نویسندگان | ||
عبدالرضا کاظمی* 1؛ الهه جهانشاهی2 | ||
1دانشیار گروه علوم ورزشی، دانشکده ادبیات و علوم انسانی، دانشگاه ولی عصر، رفسنجان، کرمان، ایران | ||
2گروه فیزیولوژی ورزشی، دانشکده ادبیات و علوم انسانی، دانشگاه آزاد اسلامی، کرمان، - مرکز تحقیقات فیزیولوژی، دانشگاه علوم پزشکی کرمان، کرمان، ایران | ||
تاریخ دریافت: 20 بهمن 1397، تاریخ بازنگری: 05 اردیبهشت 1398، تاریخ پذیرش: 11 تیر 1398 | ||
چکیده | ||
سابقه و هدف: مسیر /Fn14 Tweak پاسخهای فیزیولوژیکی مختلف شامل بقا سلول، تکثیر، تمایز، رگزایی، مهاجرت و آپوپتوز را تنظیم میکند. هدف پژوهش حاضر بررسی اثر لیگاسیون عصب نخاعی بر بیان ژنهای Tweakو Fn14 عضله EDL موشهای نر ویستار پس از تمرین HIT بود. مواد و روشها: بدین منظور، 24 موش نر ویستار در 2 گروه 12 تایی کنترل (C) و تمرین (HIT) قرار گرفتند. گروهتمرین بعد از یک هفته آشناسازی برنامه 4 هفته HIT را انجام دادند. سپس به طور تصادفی ساده به دو گروه 6 تایی تمرین (HIT) و گروه لیگاسیون عصب نخاعی (HIT-SNL) قرار گرفتند. همزمان گروه کنترل نیز به دو گروه 6 تایی کنترل (C) و لیگاسیون عصب نخاعی (C-SNL) تقسیم شدند. 4 هفته پس از SNL موشها قربانی و عضله EDL و نعلی استخراج و بیان ژنها به روش کمیسازی دادهها Real-time PCR اندازهگیری شد و با استفاده از آزمون تحلیل واریانس دو راهه دادهها مورد تجزیه و تحلیل قرار گرفت. یافتهها: نتایج نشان داد کاهش فعالیت بدنی به شکل SNL سبب افزایش معنیداری بیان ژنهای Tweakو Fn14 میشود (به ترتیب 0001/0=P و 002/0=P). همچنین انجام تمرین HIT قبل از SNL در گروه تمرین- SNL بهطور قابل ملاحظهای بیان ژنهای Tweak و Fn14 را نسبت به گروه کنترل-SNL کاهش میدهد (به ترتیب 0001/0=P و 001/0=P). علاوه بر این، یافتهها نشان میدهد SNL اثر معنیداری بر نسبت وزن عضله نعلی به طول درشتنی دارد (01/0=P). از طرف دیگر انجام تمرینات HIT قبل از SNL سبب افزایش معنیدار آن شد (03/0=P). نتیجهگیری: کاهش فعالیت بدنی به شکل لیگاسیون با افزایش بیان ژنهای Tweak و Fn14 همراه بود.از طرف دیگر تمرین تناوبی شدید در کاهش ژنهای آتروفیک موثر بوده است. با توجه به این یافتهها، انجام تمرینات HIT قبل از ابتلا به بی فعالیتی بتواند روند آتروفی عضلانی را کاهش دهد. | ||
کلیدواژهها | ||
لیگاسیون عصب نخاعی؛ ژن Tweak؛ ژن Fn14 و تمرین تناوبی شدید | ||
عنوان مقاله [English] | ||
Effect of Spinal Nerve Ligation on The Expression of Tweak and Fn14 Genes in EDL Mucsle of Wistar Rats After HIT Training | ||
نویسندگان [English] | ||
Abdolreza Kazemi1؛ Elahe Jahanshahi2 | ||
1Department of Physical Education and Sport Sciences, Faculty of Literature and Humanities, Vali-e-Asr University, Rafsanjan, Iran. | ||
2Department of Physical Education and Sport Science, Kerman Branch, Islamic Azad University, Kerman, Iran. & Physiology Research Center, Kerman University of Medical, Kerman, Iran | ||
چکیده [English] | ||
Background and Purpose: The Tweak/Fn14 pathway regulated various physiological responses including cell survival, proliferation, differentiation, angiogenesis, migration and apoptosis. The purpose of the present study was to investigate the effect of SNL on the expression of Tweak and Fn14 genes in the EDL muscle of Wistar rats after HIT training. Materials and methods: For this purpose, 24 male Wistar rats were divided into 2 groups of control (C) (n=12) and training (HIT) (n=12). After one-week familiarization, training group participate in four HIT training. Then, they were randomly assigned to HIT (n=6) and HIT-SNL (n=6) groups. At the same time, the control group was divided into two groups: control (C) (n=6) and SNL (C-SNL) (n=6). 4 weeks after the SNL, wistar rats were sacrificed then EDL and soleuse muscle exetracted.Then gene expressions of Tweak and Fn14 measured with Real time PCR technique. Data were analyzed using 2-way ANOVA. Results: The results showed that inactivity via SNL has a significant increased of the expression of Tweak and Fn14 genes (P=0.000and P=0.002, respectively). Also, performed before SNL reduced the expression of Tweak and Fn14 genes in SNL-T compared with SNL-C (P=0.0001 and P=0.001 respectively). In addition, the findings indicated that SNL had a significant effect on the weight of soleuse muscle mass/ tibia length (P=0.01). On the other hand, HIT training before SNL significantly increased ratio weight soleuse muscle mass/ tibia length (P=0.03). Conclusion: The decrease in activity by SNL is associated with increased in expression of Tweak and Fn14 genes. On the other hand, HIIT training have been effective in reducing atrophic genes. According to these findings, performing HIT training before inactivity can reduced the muscular atrophy process. | ||
کلیدواژهها [English] | ||
Spinal Nerve Ligation, Tweak gene, Fn14 gene, High Intensity Interval Training | ||
مراجع | ||
##Verhees KJ, Schols AM, Kelders MC, Op den Kamp CM, van der Velden JL, Langen RC. 2011. Glycogen synthase kinase-3β is required for the induction of skeletal muscle atrophy. Am J Physiol Cell Physiol. 301: 995-1007.##Fanzani A, Conraads VM, Penna F, Martinet W. 2012. Molecular and cellular mechanisms of skeletal muscle atrophy: an update. Journal of cachexia, sarcopenia and muscle. J Cachexia Sarcopenia Muscle. 3(3): 163-179.## Jespersen, J., Nedergaard, A., Andersen, L., Schjerling, P. & Andersen, J. 2011. Myostatin Expression during Human Muscle Hypertrophy and Subsequent Atrophy: Increased Myostatin with Detraining Scand J Med Sci Sports. ;21(2):215-23.##Paul PK1, Gupta SK, Bhatnagar S, Panguluri SK, Darnay BG, Choi Y, et al. 2010. Targeted ablation of TRAF6 inhibits skeletal muscle wasting in mice. J Cell Biol. 191(7):1395-411.##Winkles, J.A. 2008. The TWEAK–Fn14 cytokine–receptor axis: discovery, biology and therapeutic targeting. Nat Rev Drug Discov. 7(5): 411-425.##Kumar, A., S. Bhatnagar, and P.K. Paul. 2012. TWEAK and TRAF6 regulate skeletal muscle atrophy. Curr Opin Clin Nutr Metab Care. 15(3):233-9 .##Dogra C, Changotra H, Mohan S, Kumar A. 2006. Tumor necrosis factor-like weak inducer of apoptosis inhibits skeletal myogenesis through sustained activation of nuclear factor-κB and degradation of MyoD protein. J Biol Chem. 281(15):10327-10336.##Dogra C, Hall SL, Wedhas N, Linkhart TA, Kumar A. 2007.Fibroblast growth factor inducible 14 (Fn14)is required forthe expression of myogenicregulatory factors and differentiation of myoblasts into myotubes. Evidence for TWEAKindependent functions of Fn14 during myogenesis. J Biol Chem.. 282(20):15000-10.##Clarke BA, Drujan D, Willis MS, Murphy LO, Corpina RA, Burova E, et al. 2007. The E3 Ligase MuRF1 degrades myosin heavy chain protein in dexamethasone-treated skeletal muscle. Cell Metab. 6(5):376-85.##Bhatnagar S1, Mittal A, Gupta SK, Kumar A. 2012. TWEAK causes myotube atrophy through coordinated activation of ubiquitin‐proteasome system, autophagy, and caspases. J Cell Physiol. 227(3):1042-51.##Peterson JM1, Bakkar N, Guttridge DC. 2011. NF-kB Signaling in Skeletal Muscle Health and Disease. Curr Top Dev Biol. 96:85-119.##Mittal A1, Bhatnagar S, Kumar A, Lach-Trifilieff E, Wauters S, Li H, et al. 2010. The TWEAK–Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice. J Cell Biol. 188(6):833-49.##Wu, C.-L., S.C. Kandarian, and R.W. Jackman. 2011. Identification of genes that elicit disuse muscle atrophy via the transcription factors p50 and Bcl-3. PloS one. 6(1):e16171.##Hindi SM1, Mishra V, Bhatnagar S, Tajrishi MM, Ogura Y, Yan Z, et al. 2014. Regulatory circuitry of TWEAK-Fn14 system and PGC-1α in skeletal muscle atrophy program. FASEB J. 28(3):1398-1411.##Tajrishi MM, Sato S, Shin J, Zheng TS, Burkly LC, Kumar A.2014. The TWEAK–Fn14 dyad is involved in age-associated pathological changes in skeletal muscle. Biochem Biophys Res Commun. 446(4):1219-1224.##Meng, S.-J. and L.-J. Yu. 2010. Oxidative stress, molecular inflammation and sarcopenia. Int J Mol Sci. 11(4):1509-26.##Sheffield-Moore M, Yeckel CW, Volpi E, Wolf SE, Morio B, Chinkes DL, et al. 2004. Postexercise protein metabolism in older and younger men following moderate-intensity aerobic exercise. Am J Physiol Endocrinol Metab. 287(3): E513-E522.##Raue U, Slivka D, Jemiolo B, Hollon C, Trappe S. 2006. Myogenic gene expression at rest and after a bout of resistance exercise in young (18–30 yr) and old (80–89 yr) women. J Appl Physiol . 101(1):53-59.##Cunha TF, Bacurau AV, Moreira JB, Paixão NA, Campos JC, Ferreira JC,et al. 2012. Exercise training prevents oxidative stress and ubiquitin-proteasome system overactivity and reverse skeletal muscle atrophy in heart failure. PLoS One. 7(8):e41701.##Shefer G, Rauner G, Yablonka-Reuveni Z, Benayahu D. 2010. Reduced satellite cell numbers and myogenic capacity in aging can be alleviated by endurance exercise. PLoS One. 5(10): e13307-e13307.##Gibala MJ1, Little JP, van Essen M, Wilkin GP, Burgomaster KA, et al. 2006 Short‐term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance. J Physiol. 575 (Pt 3):901-11.##Snijders, T., L.B. Verdijk, and L.J. van Loon. 2009. The impact of sarcopenia and exercise training on skeletal muscle satellite cells. Ageing Res Rev. 8(4):328-338.##Ferreira JC1, Bacurau AV, Bueno CR Jr, Cunha TC, Tanaka LY, Jardim MA, et al. 2010. Aerobic exercise training improves Ca2+ handling and redox status of skeletal muscle in mice. Exp Biol Med (Maywood) . 235(4): 497-505.##Kim SH, Chung JM. 1992. An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat. Pain. 50(3): 355-63.##Hafstad AD, Boardman NT, Lund J, Hagve M, Khalid AM, Wisloff U, et al. 2011. High intensity interval training alters substrate utilization and reduces oxygen consumption in the heart. J Appl Physiol. 111(5):1235-41.##Tal M, Bennett GJ. 1994. Extra–territorial pain in rat with a peripheral mononeuropathy: mechano–hyperalgesia and mechano – allodynia in the territory of an uninjerd nerve. Pain. 57: 375-382.##Nilwik, R., Snijders, T., Leenders, M., Groen, B. B., Van Kranenburg, J., Verdijk, L. B. & Van Loon, L. J. 2013. The Decline In Skeletal Muscle Mass With Aging Is Mainly Attributed To A Reduction In Type Ii Muscle Fiber Size. Experimental Gerontology. 48, 492-498.##Muller, F. L., Song, W., Jang, Y. C., Liu, Y., Sabia, M., Richardson, A. & Van Remmen, H. Denervation-Induced Skeletal Muscle Atrophy Is Associated With Increased Mitochondrial Ros Production. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2007; 293, R1159-R1168.##Rowan, S. L., Rygiel, K., Purves-Smith, F. M., Solbak, N. M., Turnbull, D. M. & Hepple, R. T. 2012. Denervation Causes Fiber Atrophy and Myosin Heavy Chain Co-Expression in Senescent Skeletal Muscle. Plos One; 7, E29082.##Verdijk, L.B., et al. 2007. Satellite cell content is specifically reduced in type II skeletal muscle fibers in the elderlyAmerican Journal of Physiology-Endocrinology and Metabolism; 292(1): p. E151-E157.##Bonaldo, P. & Sandri, M. Cellular and Molecular Mechanisms of Muscle Atrophy. Disease Models & Mechanisms, 2013; 6, 25-39.##Sandri, M., Barberi, L., Bijlsma, A., Blaauw, B., Dyar, K., Milan, G., Mammucari, C. 2013. Meskers, C., Pallafacchina, G. & Paoli, A. Signalling Pathways Regulating Muscle Mass in Ageing Skeletal Muscle. The Role of the Igf1-Akt-Mtor-Foxo Pathway. Biogerontology. 14:303-323.##Tajrishi, M.M., Sato, S., Shin, J., Zheng, T.S., Burkly, L.C., Kumar, A. 2014. The TWEAK–Fn14 dyad is involved in age-associated pathological changes in skeletal muscle. Biochemival and Biophysical Research Communication.446(4): 1219-1224.##Mittal, A., Bhatnagar, S., Kumar, A., Lach-Trifilieff, E., Wauters, S., Li, H., Makonchuk, D.Y., Glass, D.J., Kumar, A. 2010. The TWEAK–Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice. Journal of Cellular Biology. 188(6): 833-49.##Shi, J., Jiang, B., Qiu, Y., Guan, J., Jain, M., Cao, X., Bauer, M., Su, L., Burkly , L.C., Leone, T.C., Kelly, D.P., Liao, R. 2013. PGC1alpha plays a critical role in TWEAK-induced cardiac dysfunction. PLoS One. 8(1): e54054.##Kazemi A. 2018. The effect of the mechanical unloading of lower limb on MST1 and Atrogin1 gene expression in Plantaris and soleus muscles of Wistar rats. Journal of Knowledge & Health 13(3):33-41.##Gomes, AV., Waddell, DS., Siu, R., Stein, M., Dewey, S., Furlow, J.D., Bodine, S.C. 2012. Upregulation of proteasome activity in muscle RING finger 1-null mice following denervation. FASEB Journal. 26(3): 2886-99.##Arbat-Plana, A., Cobianchi, S., Herrando-Grabulosa, M., Navarro, X., Udina, E. 2017. Endogenous modulation of TrkB signaling by treadmill exercise after peripheral nerve injury. Neuroscience. 340: 188-200.##English, A.W., Wilhelm, J.C., Sabatier, M.J. 2011. Enhancing recovery from peripheral nerve injury using treadmill training. Annals of Anatomy.193(4): 354-61.##Gleeson, M., Bishop, N. C., Stensel, D. J., Lindley, M. R., Mastana, S. S. & Nimmo, M. A. 2011. The Anti-Inflammatory Effects Of Exercise: Mechanisms and implications for the prevention and treatment of disease. Nature Reviews Immunology. 11(9): 607-615.##Moreira, J.B., Bechara, L.R., Bozi, L.H., Jannig, P.R., Monteiro, A.W., Dourado, P.M., Wisløff, U., Brum, P.C. 2013. High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats. Journal of Applied Physiology. 114(8): 1029-41.##Little, J.P., Safdar, A., Bishop, D., Tarnopolsky, MA., Gibala, M.J. 2011. 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. 300(6): R1303-10.##Gurd, B.J., Perry, C.G., Heigenhauser, G.J., Spriet, L.L., Bonen, A. 2010. High-intensity interval training increases SIRT1 activity in human skeletal muscle. Applied Physiology, Nutrition and Metabolism. 35(3): 350-7.## | ||
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