اثر تمرین تداومی و تناوبی شدید بر بیان ژن‌های Bcl-2،Bax و پروتئین P-53 بافت بطن چپ موش صحرائی نرمبتلا به دیابت نوع2

نوع مقاله : مقاله پژوهشی

نویسندگان

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

2 استاد گروه فیزیولوژی ورزشی،دانشکده تربیت بدنی و علوم ورزشی، واحد تهران مرکزی، دانشگاه آزاد اسلامی، تهران، ایران

3 دانشیار فیزیولوژی ورزشی ،دانشکده تربیت بدنی وعلوم ورزشی،واحد تهران مرکزی ،دانشگاه آزاد اسلامی ،تهران ،ایران

چکیده

مقدمه: هدف از این مطالعه مقایسه اثر 8 هفته تمرین تداومی و تناوبی شدید بر بیان ژن­های Bcl-2،Bax  و سنتز پروتئین P-53 در بافت بطن چپ موش صحرائی نرمبتلا به دیابت نوع2 بود.
روش کار: 24 سر موش نر دیابتی به سه گروه 8 تایی؛  تمرین تدوامی(CT)، تناوبی شدید(HIIT) و کنترل(C) تقسیم شدند. القاء دیابت به صورت پلت با رژیم غذایی پر چرب به مدت 24 هفته انجام شد. برای سنجش گلوکز پلاسما از روش گلوکز اکسیداز، اندازه گیری مقادیر انسولین از روش الایزا و شاخص مقاومت به انسولین از روش HOMA-IR استفاده شد. همچنین جهت تعیین بیان ژن­های Bax،Bcl-2  و سنتز پروتئین P-53 از روش PCRReal time- استفاده شد.
نتایج: بیان ژن Bcl-2  در گروه HIIT نسبت به گروه تمرین  CT(002/0P=) و کنترل (000/0P=) و در گروه CT نسبت به گروه کنترل (033/0P=) افزایش معناداری نشان داد. ژن Bax نیز در هر دو گروه تمرین  HIIT(000/0P= ) و CT (009/0P=) نسبت به گروه کنترل کاهش معناداری نشان داد. سنتز پروتئین p-53 در گروه HIIT نسبت به گروه تمرین CT (012/0P=) و کنترل (000/0P=) کاهش معناداری را نشان داد.
نتیجه گیری: بر اساس یافته­های به دست آمده 8 هفته تمرین تناوبی شدید با تاثیر بالاتر بر افزایش بیان ژن Bcl-2 و کاهش سنتز پروتئین P-53 احتمالا می­تواند آپوپتوز را در بطن چپ موش­های مبتلا به دیابت بهبود بخشد که  فیبروز و اختلال  عملکردی را در بافت قلب کاهش داده و احتمالا می­تواند عامل موثری در کاهش کاردیومیوپاتی ناشی از دیابت باشد.

کلیدواژه‌ها

عنوان مقاله [English]

Effect of High Intensity Interval Training and Continous Training on the Gene Expression of Bcl2, Bax and P-53 Protein in the Left Ventricle type 2 diabetes of Male Rats

نویسندگان [English]

  • Alireza Safar nezhad 1
  • Maghsoud Peeri 2
  • Hasan Matin Homaee 3
1 Department of Exercise physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
2 2- Professor, Department of exercise physiology, Faculty of physical education and sport science, Islamic Azad University, Central Tehran Branch, Tehran, Iran.
3 Associate professor , Department of exercise physiology, Faculty of physical education and sport science, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
چکیده [English]

Abstract
Background: The purpose of this study was the Effect of High-Intensity Interval Training and Continous Training on the Gene Expression of Bcl2, Bax and  P-53 Protein in the Left Ventricle type 2 diabetes of Male Rats
Material and Methods: 24 male diabetic rats were divided into 3 groups of 8; High-intensity intensity interval training (HIIT), Moderate training (CT), and Control (C). Diabetes was induced in a pellet with a high-fat diet (30% fat and 25% fructose) for 24 weeks. Glucose oxidase was used to measure glucose in plasma using and the HOMA-IR method was used to measure insulin resistance index. PCR-Real time was used to determine the expression of BAX and BCL-2 genes and P-53 Protein Synthesis.
Results: geneexperision of Bcl-2 was significantly increased in the HIIT group compared to the CT (P=0/002) and control groups (p=0/000) and in the CT group compared to the Control group (p=0/033). Bax gene was significantly decreased in both groups HIIT(p=0/000) and CT(p=0/009) compared to the Control group (P=0/0001). P-53 protein synthesis was significantly in HIIT compared to CT (p=0/012) and control group (p=0/000).
Conclusion: Based on the findings, 8 weeks of intensity interval training with a higher effect on increasing Bcl-2 gene expression and decreased P-53 protein synthesis may improve left ventricular apoptosis in diabetic rats which reduces fibrosis and dysfunction in the heart tissue and may be an effective factor in reducing diabetic cardiomyopathy.

کلیدواژه‌ها [English]

  • Cardiomyocyte
  • Apoptosis
  • BAX
  • BCL2
  • P-53

مراجع

  1. Castellar A, Remedio RN, Barbosa RA, Gomes RJ, Caetano FH. Collagen and reticular fibers in left ventricular muscle in diabetic rats: Physical exercise prevents its changes?. Tissue and Cell. 2011 Feb 1;43(1):24-8.
  2. Shimizu M, Umeda K, Sugihara N, Yoshio H, Ino H, Takeda R, Okada Y, Nakanishi I. Collagen remodelling in myocardia of patients with diabetes. Journal of clinical pathology. 1993 Jan 1;46(1):32-6.
  3. Powers SK, Demirel HA, Vincent HK, Coombes JS, Naito H, Hamilton KL, Shanely RA, Jessup J. Exercise training improves myocardial tolerance to in vivo ischemia-reperfusion in the rat. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 1998 Nov 1;275(5):R1468-77.
  4. Lorenzo O, Picatoste B, Ares-Carrasco S, Ramirez E, Egido J, Tunon J. Potential role of nuclear factor κB in diabetic cardiomyopathy. Mediators of inflammation. 2011;2011.
  5. Lu K, Shen Y, He J, Liu G, Song W. Berberine inhibits cardiac fibrosis of diabetic rats. Xi bao yu fen zi mian yi xue za zhi= Chinese journal of cellular and molecular immunology. 2016 Oct 1;32(10):1352-5.
  6. Grundy SM, Benjamin IJ, Burke GL, Chait A, Eckel RH, Howard BV, Mitch W, Smith Jr SC, Sowers JR. Diabetes and cardiovascular disease: a statement for healthcare professionals from the American Heart Association. Circulation. 1999 Sep 7;100(10):1134-46.
  7. Xu X, Wan W, Ji L, Lao S, Powers AS, Zhao W, Erikson JM, Zhang JQ. Exercise training combined with angiotensin II receptor blockade limits post-infarct ventricular remodelling in rats. Cardiovascular research. 2008 Jun 1;78(3):523-32.
  8. Fadini GP, Iori E, Marescotti MC, de Kreutzenberg SV, Avogaro A. Insulin-induced glucose control improves HDL cholesterol levels but not reverse cholesterol transport in type 2 diabetic patients. Atherosclerosis. 2014 Aug 1;235(2):415-7.
  9. Marzetti E, Privitera G, Simili V, Wohlgemuth SE, Aulisa L, Pahor M, Leeuwenburgh C. Multiple pathways to the same end: mechanisms of myonuclear apoptosis in sarcopenia of aging. TheScientificWorldJOURNAL. 2010 Feb 19;10:340-9.
  10. Asiri YA. Probucol attenuates cyclophosphamide-induced oxidative apoptosis, p53 and Bax signal expression in rat cardiac tissues. Oxidative Medicine and Cellular Longevity. 2010 Sep 1;3(5):308-16.
  11. Sahin E, DePinho RA. Axis of ageing: telomeres, p53 and mitochondria. Nature reviews Molecular cell biology. 2012 Jun;13(6):397-404.
  12. Tanoorsaz S, Behpour N, Tadibi V. Investigating the Effect of mid-term of aerobic exercise on apoptosis biomarkers in the cardiomyocytes of streptozotocin-induced diabetic rats. Journal of Fasa University of Medical Sciences. 2018;7(4):488-97.
  13. Luedde M, Lutz M, Carter N, Sosna J, Jacoby C, Vucur M, Gautheron J, Roderburg C, Borg N, Reisinger F, Hippe HJ. RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction. Cardiovascular research. 2014 Jul 15;103(2):206-16.
  14. Köhler C, Orrenius S, Zhivotovsky B. Evaluation of caspase activity in apoptotic cells. Journal of immunological methods. 2002 Jul 1;265(1-2):97-110.
  15. Estes RR, Malinowski AM, Piacentini M, Thrush D, Salley E, Losey C, Hayes E. The effect of high intensity interval run training on cross-sectional area of the vastus lateralis in untrained college students. International journal of exercise science. 2017;10(1):137.
  16. Kim DY, Jung SY, Kim CJ, Sung YH, Kim JD. Treadmill exercise ameliorates apoptotic cell death in the retinas of diabetic rats. Molecular medicine reports. 2013 Jun 1;7(6):1745-50.
  17. Gibala MJ, Little JP, MacDonald MJ, Hawley JA. Physiological adaptations to low‐volume, high‐intensity interval training in health and disease. The Journal of physiology. 2012 Mar 1;590(5):1077-84.
  18. Touvra AM, Volaklis KA, Spassis AT, Zois CE, Douda HT, Kotsa K, Tokmakidis SP. Combined strength and aerobic training increases transforming growth factor-β1 in patients with type 2 diabetes. Hormones. 2011 Apr;10(2):125-30.
  19. Aboutaleb N, Shamsaei N, Khaksari M, Erfani S, Rajabi H, Nikbakht F. Pre-ischemic exercise reduces apoptosis in hippocampal CA3 cells after cerebral ischemia by modulation of the Bax/Bcl-2 proteins ratio and prevention of caspase-3 activation. The Journal of Physiological Sciences. 2015 Sep;65(5):435-43.
  20. Khakdan S, Delfan M, Heydarpour Meymeh M, Kazerouni F, Ghaedi H, Shanaki M, Kalaki-Jouybari F, Gorgani-Firuzjaee S, Rahimipour A. High-intensity interval training (HIIT) effectively enhances heart function via miR-195 dependent cardiomyopathy reduction in high-fat high-fructose diet-induced diabetic rats. Archives of physiology and biochemistry. 2020 May 26;126(3):250-7.
  21. PITHON-CURI TN. Aprogram Of Moderate Physical Training For Wistar Rats Based On Maximal Oxygen Consumption. Journal of strength and conditioning research. 2007;21(3):000-.
  22. Kadoglou NP, Perrea D, Iliadis F, Angelopoulou N, Liapis C, Alevizos M. Exercise reduces resistin and inflammatory cytokines in patients with type 2 diabetes. Diabetes care. 2007 Mar 1;30(3):719-21.
  23. Jing E, Emanuelli B, Hirschey MD, Boucher J, Lee KY, Lombard D, Verdin EM, Kahn CR. Sirtuin-3 (Sirt3) regulates skeletal muscle metabolism and insulin signaling via altered mitochondrial oxidation and reactive oxygen species production. Proceedings of the national academy of sciences. 2011 Aug 30;108(35):14608-13.
  24. Henle T. AGEs in foods: do they play a role in uremia?. Kidney international. 2003 May 1;63:S145-7.
  25. Hofmann MA, Schiekofer S, Isermann B, Kanitz M, Henkels M, Joswig M, Treusch A, Morcos M, Weiss T, Borcea V, Khalek AA. Peripheral blood mononuclear cells isolated from patients with diabetic nephropathy show increased activation of the oxidative-stress sensitive transcription factor NF-kB. Diabetologia. 1999 Jan;42(2):222-32.
  26. Vettor R, Valerio A, Ragni M, Trevellin E, Granzotto M, Olivieri M, Tedesco L, Ruocco C, Fossati A, Fabris R, Serra R. Exercise training boosts eNOS-dependent mitochondrial biogenesis in mouse heart: role in adaptation of glucose metabolism. American Journal of Physiology-Endocrinology and Metabolism. 2014 Mar 1;306(5):E519-28.
  27. Golbidi S, Badran M, Laher I. Antioxidant and anti-inflammatory effects of exercise in diabetic patients. Experimental diabetes research. 2011 Oct 11;2012.
  28. Borges JP, Lessa MA. Mechanisms involved in exercise-induced cardioprotection: a systematic review. Arquivos brasileiros de cardiologia. 2015 Jul;105(1):71-81.
  29. Oliveira NL, Ribeiro F, Silva G, Alves AJ, Silva N, Guimaraes JT, Teixeira M, Oliveira J. Effect of exercise-based cardiac rehabilitation on arterial stiffness and inflammatory and endothelial dysfunction biomarkers: a randomized controlled trial of myocardial infarction patients. Atherosclerosis. 2015 Mar 1;239(1):150-7.
  30. Scheffer DL, Silva LA, Tromm CB, da Rosa GL, Silveira PC, de Souza CT, Latini A, Pinho RA. Impact of different resistance training protocols on muscular oxidative stress parameters. Applied Physiology, Nutrition, and Metabolism. 2012 Dec;37(6):1239-46.
  31. Launay T, Momken I, Carreira S, Mougenot N, Zhou XL, De Koning L, Niel R, Riou B, Billat V, Besse S. Acceleration-based training: A new mode of training in senescent rats improving performance and left ventricular and muscle functions. Experimental gerontology. 2017 Sep 1;95:71-6.
  32. Holloway TM, Bloemberg D, Da Silva ML, Simpson JA, Quadrilatero J, Spriet LL. High intensity interval and endurance training have opposing effects on markers of heart failure and cardiac remodeling in hypertensive rats. PloS one. 2015 Mar 24;10(3):e0121138.
مجله دانشکده پزشکی دانشگاه علوم پزشکی مشهد
دوره 63، شماره 5
آذر و دی 1399
صفحه 2769-2881

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