نوع مقاله : مقاله پژوهشی Released under CC BY-NC 4.0 license I Open Access I

نویسندگان

1 . دانشیار فیزیولوژی ورزشی، گروه علوم ورزشی، دانشکدۀ ادبیات و علوم انسانی، دانشگاه ولی‌عصر (عج) ، رفسنجان، ایران

2 الف) دانشجوی کارشناس ارشد، گروه فیزیولوژی ورزشی، دانشگاه آزاد اسلامی، کرمان، ایران، ب) مرکز تحقیقات فیزیولوژی، دانشگاه علوم پزشکی کرمان، کرمان ایران

چکیده

هدف از پژوهش حاضر بررسی اثر لیگاسیون عصب نخاعی (SNL) بر بیان ژن‌های TRAF6 و MuRF1 عضلة نعلی موش‌های نر ویستار پس از یک دوره تمرین تناوبی شدید بود. بدین‌منظور، 24 سر موش نر ویستار در 2 گروه 12 تایی کنترل (C) و تمرین (HIT) قرار گرفتند. گروه تمرین بعد از یک هفته آشناسازی برنامۀ 4 هفته تمرین تناوبی شدید را انجام دادند. سپس به‌طور تصادفی در 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 شدند و عضلة نعلی استخراج و به‌وسیلۀ روش کمی‌سازی داده‌ها Real-time Pcr بیان ژن‌ها اندازه‌گیری شد. نتایج نشان داد که کاهش فعالیت به شکل SNL اثر معنا‌داری بر بیان ژن‌های TRAF6 و MuRF1 دارد (به‌ترتیب 0001/0=P و 0001/0=P). همچنین انجام تمرین ورزشی شدید قبل از SNL به‌طور چشمگیری بیان TRAF6 و MuRF1 را کاهش می‌دهد (به‌ترتیب 003/0=P و 0001/0=P). علاوه‌بر این، یافته‌ها نشان می‌دهد که SNL اثر معنا‌داری بر نسبت وزن عضلة نعلی به طول درشت‌نی داشته است (01/0=P). از طرف دیگر، انجام تمرینات HIT قبل از SNL سبب افزایش معنا‌دار در این نسبت شد (03/0=P).  نتایج نشان داد کاهش فعالیت به شکل SNL با افزایش بیان ژن‌های TRAF6 و MuRF1 همراه است که احتمالاً می‌تواند در تغییر تودة عضلانی نیز درگیر باشد. با توجه به اینکه انجام تمرینات با شدت بالا بیان این ژن‌ها را کاهش می‌دهد، این تمرینات می‌توانند به‌منظور حفظ تودة عضلانی مطلوب‌تر قبل از بی‌فعالیتی بدنی به‌کار روند.

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

Effect of Spinal Nerve Ligation (SNL) on the Expression of TRAF6 and MuRF1 Genes in soleus Mucsle of Wistar Rats after HIT Training

نویسندگان [English]

  • Abdolreza Kazemi 1
  • Alireza Saeed 2

1 Associate Professor in Exercise Physiology, Department of Sport Sciences, Faculty of Literature and Humanities, Vali E-Asr University, Rafsanjan, Iran

2 . a) MSc Student, Department of Exercise Physiology, Islamic Azad University, Kerman, Iran, b) Physiology Research Center, Kerman University of Medical Sciences, Kerman, Iran

چکیده [English]

The purpose of the present study was to investigate the effect of SNL on the expression of TRAF6 muRF1 genes in the Soleus muscle of Wistar rats after HIT traning. For this purpose, 24 male 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 spinal cord nerve (C-SNL) (n=6). 4 weeks after the SNL, wistar rats were sacrificed and soleuse muscle exetracted.Then Gene expressions of MuRF1 and TRAF6 measured Real time PCR technique. The results showed that inactivity by SNL has a significant effect on the expression of TRAF6 and MuRF1 genes (P=0.0001 and P=0.0001, respectively). Also, performed before SNL reduced the expression of TRAF6 and MuRF1 (P=0.003 and P=0.0001 respectively). In addition, the findings indicated that SNL had a significant effect on the weight of Soleus muscle mass/ tibia length (P=0.01). On the other hand, HIT training before SNL significantly increased weight of Soleus muscle mass/ tibia length (P = 0.03). Therefore, the decrease in activity by SNL is associated with increased in expression of TRAF6 and MuRF1 genes, which may also be involved in muscle mass changes. Regarding the fact that performing HIT reduces the expression of these genes in soleus muscle, these training can be used to maintain obtimal muscle mass before physical activity.

کلیدواژه‌ها [English]

  • SNL
  • تمرین تناوبی
  • MuRF1
  • TRAF6
1.   Bize, R., J.A. Johnson, and R.C. Plotnikoff, Physical activity level and health-related quality of life in the general adult population: a systematic review. Preventive medicine, 2007. 45(6): p. 401-415.
2.   Europe, W., Steps to health: a european framework to promote physical activity for health. Europe: WHO, 2007.
3.   Warburton, D.E., C.W. Nicol, and S.S. Bredin, Health benefits of physical activity: the evidence. Cmaj, 2006. 174(6): p. 801-809.
4.   Verhees, K.J., et al., Glycogen synthase kinase-3β is required for the induction of skeletal muscle atrophy. American Journal of Physiology-Cell Physiology, 2011. 301(5): p. C995-C1007.
5.   Fanzani, A., et al., Molecular and cellular mechanisms of skeletal muscle atrophy: an update. Journal of cachexia, sarcopenia and muscle, 2012. 3(3): p. 163-179.
6.   Jespersen, J., et al., Myostatin expression during human muscle hypertrophy and subsequent atrophy: increased myostatin with detraining. Scandinavian journal of medicine & science in sports, 2011. 21(2): p. 215-223.
7.   Paul, P.K., et al., Targeted ablation of TRAF6 inhibits skeletal muscle wasting in mice. Journal of Cell Biology, 2010. 191(7): p. 1395-1411.
8.   Chung, J.Y., et al., Molecular basis for the unique specificity of TRAF6, in TNF Receptor Associated Factors (TRAFs). 2007, Springer. p. 122-130.
9.   Zapata, J.M., S. Lefebvre, and J.C. Reed, Targeting TRAfs for therapeutic intervention, in TNF Receptor Associated Factors (TRAFs). 2007, Springer. p. 188-201.
10. Paul, P.K., et al., The E3 ubiquitin ligase TRAF6 intercedes in starvation-induced skeletal muscle atrophy through multiple mechanisms. Molecular and cellular biology, 2012. 32(7): p. 1248-1259.
11. Sun, H., et al., TRAF6 inhibition rescues dexamethasone-induced muscle atrophy. International journal of molecular sciences, 2014. 15(6): p. 11126-11141.
12. Gustafsson, T., et al., Effects of 3 days unloading on molecular regulators of muscle size in humans. Journal of applied physiology, 2010. 109(3): p. 721-727.
13. Aagaard, P., et al., Role of the nervous system in sarcopenia and muscle atrophy with aging: strength training as a countermeasure. Scandinavian journal of medicine & science in sports, 2010. 20(1): p. 49-64.
14. Sheffield-Moore, M., et al., Postexercise protein metabolism in older and younger men following moderate-intensity aerobic exercise. American Journal of Physiology-Endocrinology and Metabolism, 2004. 287(3): p. E513-E522.
15. Raue, U., et al., Myogenic gene expression at rest and after a bout of resistance exercise in young (18–30 yr) and old (80–89 yr) women. Journal of Applied Physiology, 2006. 101(1): p. 53-59.
16. Gielen, S., et al., Exercise training attenuates MuRF-1 expression in the skeletal muscle of patients with chronic heart failure independent of age: the randomized Leipzig Exercise Intervention in Chronic Heart Failure and Aging catabolism study. Circulation, 2012. 125(22): p. 2716-2727.
17. Drey, M., et al., Motoneuron loss is associated with sarcopenia. Journal of the American Medical Directors Association, 2014. 15(6): p. 435-439.
18. Glass, D.J., Signalling pathways that mediate skeletal muscle hypertrophy and atrophy. Nature cell biology, 2003. 5(2): p. 87-90.
19. Aguiar, A., et al., High-intensity physical exercise disrupts implicit memory in mice: involvement of the striatal glutathione antioxidant system and intracellular signaling. Neuroscience, 2010. 171(4): p. 1216-1227.
20. Nytrøen, K., et al., High‐Intensity Interval Training Improves Peak Oxygen Uptake and Muscular Exercise Capacity in Heart Transplant Recipients. American Journal of Transplantation, 2012. 12(11): p. 3134-3142.
21. Gillen, J.B., et al., Three minutes of all-out intermittent exercise per week increases skeletal muscle oxidative capacity and improves cardiometabolic health. PLoS One, 2014. 9(11): p. e111489.
22. Laursen, P.B. and D.G. Jenkins, The scientific basis for high-intensity interval training. Sports Medicine, 2002. 32(1): p. 53-73.
23. Miyamoto-Mikami, E., et al., Gene expression profile of muscle adaptation to high-intensity intermittent exercise training in young men. Scientific reports, 2018. 8(1): p. 1-14.
24. Winter, B., et al., High impact running improves learning. Neurobiology of learning and memory, 2007. 87(4): p. 597-609.
25. Aguiar, A.S., et al., Downhill training upregulates mice hippocampal and striatal brain-derived neurotrophic factor levels. Journal of neural transmission, 2008. 115(9): p. 1251-1255.
26. Kim, S.H. and J.M. Chung, An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat. Pain, 1992. 50(3): p. 355-363.
27. Hafstad, A.D., et al., High intensity interval training alters substrate utilization and reduces oxygen consumption in the heart. Journal of Applied Physiology, 2011. 111(5): p. 1235-1241.
28. Tal, M. and G.J. Bennett, Extra-territorial pain in rats with a peripheral mononeuropathy: mechano-hyperalgesia and mechano-allodynia in the territory of an uninjured nerve. Pain, 1994. 57(3): p. 375-382.
29. Nilwik, R., et al., The decline in skeletal muscle mass with aging is mainly attributed to a reduction in type II muscle fiber size. Experimental gerontology, 2013. 48(5): p. 492-498.
30. Muller, F.L., et al., Denervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS production. American journal of physiology-Regulatory, integrative and comparative physiology, 2007. 293(3): p. R1159-R1168.
31. Rowan, S.L., et al., Denervation causes fiber atrophy and myosin heavy chain co-expression in senescent skeletal muscle. PloS one, 2012. 7(1): p. e29082.
32. Verdijk, L.B., et al., Satellite cell content is specifically reduced in type II skeletal muscle fibers in the elderly. American Journal of Physiology-Endocrinology and Metabolism, 2007. 292(1): p. E151-E157.
33. Bonaldo, P. and M. Sandri, Cellular and molecular mechanisms of muscle atrophy. Disease models & mechanisms, 2013. 6(1): p. 25-39.
34. Sandri, M., et al., Signalling pathways regulating muscle mass in ageing skeletal muscle. The role of the IGF1-Akt-mTOR-FoxO pathway. Biogerontology, 2013. 14(3): p. 303-323.
35. Labeit, S., et al., Modulation of muscle atrophy, fatigue and MLC phosphorylation by MuRF1 as indicated by hindlimb suspension studies on MuRF1-KO mice. Journal of Biomedicine and Biotechnology, 2010. 2010.
36. Al-Nassan, S., et al., Chronic exercise training down-regulates TNF-α and atrogin-1/MAFbx in mouse gastrocnemius muscle atrophy induced by hindlimb unloading. Acta Histochemica et Cytochemica, 2012. 45(6): p. 343-349.
37. Labeit, S., et al., Modulation of muscle atrophy, fatigue and MLC phosphorylation by MuRF1 as indicated by hindlimb suspension studies on MuRF1-KO mice. BioMed Research International, 2010. 2010.
38. Polge, C., et al., UBE2D2 is not involved in MuRF1-dependent muscle wasting during hindlimb suspension. The international journal of biochemistry & cell biology, 2016. 79: p. 488-493.
39. Paul, P.K., et al., Targeted ablation of TRAF6 inhibits skeletal muscle wasting in mice. The Journal of cell biology, 2010. 191(7): p. 1395-1411.
40. Cai, D., et al., IKKβ/NF-κB activation causes severe muscle wasting in mice. Cell, 2004. 119(2): p. 285-298.
41. Li, H., S. Malhotra, and A. Kumar, Nuclear factor-kappa B signaling in skeletal muscle atrophy. Journal of molecular medicine, 2008. 86(10): p. 1113-1126.
42. Bilodeau, P.A., E.S. Coyne, and S.S. Wing, The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation. American Journal of Physiology-Cell Physiology, 2016. 311(3): p. C392-C403.
43. Mittal, A., et al., The TWEAK–Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice. The Journal of cell biology, 2010. 188(6): p. 833-849.
44. Wu, C.-L., S.C. Kandarian, and R.W. Jackman, Identification of genes that elicit disuse muscle atrophy via the transcription factors p50 and Bcl-3. PloS one, 2011. 6(1): p. e16171.
45. Sadri, S., G. Sharifi, and K.J. Dehkordi, Effects of high intensity interval training (up&downward running) with BCAA/nano chitosan on Foxo3 and SMAD soleus muscles of aging rat. Life Sciences, 2020: p. 117641.
46. Kazemi, A. and E. Jahanshahi, Effect of Spinal Nerve Ligation on The Expression of Tweak and Fn14 Genes in EDL Mucsle of Wistar Rats After HIT Training.