آثار پیشگیرانه دو پروتکل تمرین استقامتی تداومی و تناوبی بر بیان ژن گلکتین- 3 میوکارد در موشهای صحرایی نر ویستار متعاقب القای آنفارکتوس قلبی

محمدی مقدم, احمد; تادیبی, وحید; بهپور, ناصر; نظری, افشین

doi:10.52547/joeppa.14.1.73

آثار پیشگیرانه دو پروتکل تمرین استقامتی تداومی و تناوبی بر بیان ژن گلکتین- 3 میوکارد در موشهای صحرایی نر ویستار متعاقب القای آنفارکتوس قلبی

نوع مقاله : علمی - پژوهشی

نویسندگان

¹ گروه فیزیولوژی ورزشی، دانشکدۀ علوم ورزشی، دانشگاه رازی، کرمانشاه، ایران

² گروه فیزیولوژی، دانشکده پزشکی، دانشگاه علوم پزشکی لرستان،لرستان، ایران

10.52547/joeppa.14.1.73

چکیده

هدف: نشانگرهای زیستی حاوی اطلاعات پیش‌آگهی به‌منظور شناسایی و پیشگیری بیماری‌های قلبی‌اند. گلکتین-3 از محتمل‌ترین واسطه‌گرهای بین فعال‌سازی ماکروفاژها و فیبروز قلب است. این پژوهش به بررسی میزان بیان ژن گلکتین-3 بافت قلب موش‌های صحرایی نر ویستار به‌دنبال یک دوره تمرینات استقامتی تداومی و تناوبی می‌پردازد.
روش‌ها: در این پژوهش در نهایت 32 سر موش صحرایی در شرایط استاندارد نگهداری و به چهار گروه (گروه شاهد سالم، گروه شاهد ایسکمی، گروه تمرین تداومی و گروه تمرین تناوبی) تقسیم شدند. گروه شاهد سالم بدون القای آنفارکتوس و گروه شاهد ایسکمی پس از 8 هفته به آنفارکتوس قلبی مبتلا شدند. گروه‌های تمرینی نیز به مدت 8 هفته به تمرینات استقامتی روی نوار گردان پرداختند و پس از 48 ساعت استراحت به آنفارکتوس قلبی مبتلا شدند. یک هفته پس از القا و اطمینان از ایجاد ایسکمی، قلب موش‌های صحرایی جدا و به‌منظور اندازه‌گیری بیان ژنLGALS3 میوکارد از روش qRT-PCR استفاده شد. از آزمون تی و آزمون آنوا یکطرفه و در ادامه آزمون تعقیبی توکی با سطح معناداری 05/0 به‌منظور مقایسة گروه‌ها استفاده شد.
نتایج: یافته‌های پژوهش حاضر حاکی از افزایش معنادار بیان ژن گلکتین-3 در بافت قلب موش‌های صحرایی نر ویستار پس از القای آنفارکتوس قلبی نسبت به گروه شاهد سالم بود (05/0P<). همچنین بیان نسبی ژن مذکور در گروه شاهد ایسکمی به‌طور معناداری بالاتر از هر دو گروه‌های تمرینی بود (05/0P<). در مقایسة دو نوع تمرین، میزان نسبی بیان ژن گلکتین-3 در گروه تداومی کمتر بود (05/0P<).

کلیدواژه‌ها

عنوان مقاله [English]

Preventive effects of two continuous and interval endurance exercise protocols on myocardial Galectin-3 gene expressions in male Wistar rats following cardiac infarction induction

نویسندگان [English]

ahmad mohammadi moghaddam ¹
vahid tadibi ¹
naser behpoor ¹
afshin nazari ²

¹ Department of Sports Physiology, Faculty of Sports Sciences, Razi University, Kermanshah, Iran

² Department of Physiology, Faculty of Medicine, Lorestan University of Medical Sciences, Lorestan, Iran

چکیده [English]

Purpose: Biomarkers contain prognostic information for the identification and prevention of heart disease. Galactin-3 is one of the most probable intermediates between the activation of macrophages and cardiac fibrosis. This study investigates the expression of galectin-3 gene in the heart tissue of male Wistar rats following a period of continuous and interval endurance training.
Methods: In the present study, 32 rats were kept under standard conditions and divided into four groups (healthy control group, ischemic control group, continuous training group and interval training group). The healthy control group, without an infarction, and ischemic control group, were suffered cardiac infarction after eight weeks. The training groups have also performed endurance training on treadmill for eight weeks and were suffered cardiac infarction after 48 hours of rest. One week after induction and confidence of ischemia, the rat’s hearts were separated and qRT-PCR method was used to measure the myocardium LGALS3 gene expression. t-test and one-way ANOVA test and then Tukey's post hoc test were used with significant level 0.05 to compare the groups.
Results: The findings of this research showed a significant increase in the expression of galectin-3 gene in heart tissue of male Wistar rats after induction of myocardial infarction compared to healthy control group (P < 0.05). Also, the relative expression of this gene in the ischemia control group was significantly higher than the both training groups (P < 0.05). Comparing two types of training, the relative level of expression of galectin-3 gene was lower in the continuous group (P < 0.05).
Conclusion: Suffering from infarction leads to increase in some of the myocardial risk factors and Cardiac fibrosis. Endurance training, especially regular continuous training can moderate the increase in some of these factors.

کلیدواژه‌ها [English]

Infarction
Macrophage
Galectin-3
Interval training
Continuous training

مراجع

1. Weber KT, Pick R, Jalil JE, Janicki JS, Carroll EP. Patterns of myocardial fibrosis. J Mol Cell Cardiol. 1989; 21 (Suppl 5): 121–131.
2. Leyva F, Taylor RJ, Foley PW, Umar F, Mulligan LJ, Patel K, and et al. Left ventricular midwall fibrosis as a predictor of mortality and morbidity after cardiac resynchronization therapy in patients with nonischemic cardiomyopathy. J Am Coll Cardiol. 2012; 60(17): 1659–1667.
3. Gulati A, Jabbour A, Ismail TF, Guha K, Khwaja J, Raza S, et al. Association of fibrosis with mortality and sudden cardiac death in patients with nonischemic dilated cardiomyopathy. JAMA. 2013; 309(9): 896–908.
4. Nabeta T, Inomata T, Iida Y, Ikeda Y, Iwamoto M, Ishii S, and et al. Baseline cardiac magnetic resonance imaging versus baseline endomyocardial biopsy for the prediction of left ventricular reverse remodeling and prognosis in response to therapy in patients with idiopathic dilated cardiomyopathy. Heart Vessels. 2014; 29(6): 784–792.
5. Ho JE, Liu C, Lyass A, Courchesne P, Pencina MJ, Vasan RS, and et al. Galectin-3, a Marker of Cardiac Fibrosis, Predicts Incident Heart Failure in the Community. JACC. 2012; 60(14): 1249–1256.
6. Felker GM, Fiuzat M, Shaw LK, Clare R, Whellan DJ, Bettari L, and et al. Galectin-3 in Ambulatory Patients with Heart Failure: Results from the HF-ACTION Study. Circ Heart Fail. 2012; 5(1); 72-78.

7. De Boer RA, Yu L, Van Veldhuisen DJ. Galectin-3 in Cardiac Remodeling and Heart Failure. Curr Heart Fail Rep. 2010; 7(1): 1–8.
8. De Boer RA, Voors1 AA, Muntendam P, Van Gilst1 WH, Van Veldhuisen DJ. Galectin-3: a novel mediator of heart failure development and progression. Eur J Heart Fail. 2009; 11(9): 811–817.
9. Kramer F. Galectin-3: clinical utility and prognostic value in patients with heart failure. Res Rep Clin Cardiol. 2013; 4, 13-22.
10. Liu FT, Rabinovich GA. Galectins: regulators of acute and chronic inflammation. Ann N Y Acad Sci. 2010; 1183: 158-182.
11. Lok DJA, Van Der Meer P, De la Porte P, Lipsic E, Van Wijngaarden J, and et al. Prognostic value of galectin-3, a novel marker of fi brosis, in patients with chronic heart failure: data from the DEAL-HF study. Clin Res Cardiol. 2010; 99: 323–328.
12. Sharma UC, Pokharel S, van Brakel TJ, van Berlo JH, Cleutjens JP, Schroen B, and et al. Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction. Circulation. 2004; 110: 3121–3128.
13. Defi lippi CR, Felker GM. Galectin-3 in Heart Failure-Linking Fibrosis, Remodeling, and Progression. ECR. 2010; 6(2): 33-36.
14. Dong S and Hughes RC. Macrophage surface glycoproteins binding to galectin-3 (Mac-2-antigen). Glycoconj J. 1997; 14(2): 267-274.

Hughes RC. Secretion of the galectin family of mammalian carbohydrate binding family proteins. Biochem Biophysica Acta. 1999; 1473(1): 172-185.
16. Atabakhshian. R, Raygan. F, Kazerouni. F. Galectin-3 in fi brosis and heart failure. J Clin Exc 1393; 2(2): 36-49.
17. Iqbal N, Wentworth B, Choudhary R, Landa Ade L, Kipper B, Fard A, and et al. Cardiac biomarkers: new tools for heart failure management. Cardiovasc Diagn Ther. 2012; 2(2): 147-164.
18. Pedersen, B. K. and Saltin, B. Evidence for prescribing exercise as therapy in chronic disease. Scand J Med Sci Sports. 2006; 16 (1): 3-63.
19. Guasch E, Benito B, Qi X, et al. Atrial Fibrillation Promotion by Endurance Exercise: Demonstration and Mechanistic Exploration in an Animal Model. Jam Coll Cardiol. Epub ahead of print. 2013; 1000-1016.
20. Gay-Jordi G, Guash E, Benito B, and et al. Losartan prevents heart fi brosis induced by long-term intensive exercise in an animal model. PLoS One. 2013; 8(2): 55427.
21. La Gerche A, Burns AT, Mooney DJ, and et al. Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes. Eur Heart J. 2011; 33: 998–1006.

Grimsmo J, Grundvold I, Maehlum S, and et al. High prevalence of atrial fi brillation in long-term endurance crosscountry skiers: echocardiographic fi ndings and possible predictors – a 28–30 Years follow-up study. Eur J Cardiovasc Prev Rehabil. 2010; 17(1): 100–105.
23. Conraads VM, Beckers P, Vaes J, Martin M, Van Hoof V, De Maeyer C, and et al. Combined endurance/resistance training reduces NT-proBNP levels in patients with chronic heart failure. Europ Heart J. 2004; 25(20): 1797-1805.

Robert Ha¨ttasch, Sebastian Spethmann, Rudolf A de Boer, Willem PT Ruifrok, Sebastian Schattk and et al. Galectin-3 increase in endurance athletes. European Journal of Preventive Cardiology. 2014; 21(10): 1192-1199.
25. Gian Luca Salvagno, Federico Schena, Matteo Gelati, Elisa Danese, Gianfranco Cervellin and et al. The concentration of high-sensitivity troponin I, galectin-3 and NT-proBNP substantially increase after a 60-km ultramarathon. Clin Chem Lab Med. 2014; 52(2): 267–272.
26. Nocon M, Hiemann T, Muller-Riemenschneider F, Thalau F, Roll S, Willich SN. Association of physical activity with all-cause and cardiovascular mortality: a systematic review and meta-analysis. Eur J Cardiovasc Prev Rehabil. 2008; 15(3): 239–246.
27. Schlüter K.D, Schreckenberg R, and da Costa Rebelo R.M. Interaction between exercise and hypertension in spontaneously hypertensive rats: a meta-analysis of experimental studies. Hypertens. Res. 2010; 33(11): 1155–1161.
28. Jakovljević VLj, Zlatković M, Cubrilo D, Pantić I, Djurić DM. The effects of progressive exercise on cardiovascular function in elite athletes: focus on oxidative stress. Acta Physiol Hung. 2011; 98(1): 51-58.
29. Guide for the care and use of laboratory animals. 8thEdition. Washington DC: The National Academies Press. 2011.

30. Chilibeck P.D, Bell G.J, Farrar R.P, Martin T.P, Higher mitochondrial fatty acid oxidation following interval versus continuous endurance exercise training. Can. J. Physiol. Pharmacol. 1998; 76 (9): 891–894.
31. Lau Y.S, Patki G, Das-Panja K, Le W.D, Ahmad S.O. Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration. Eur. J. Neurosci. 2011; 33 (7): 1264-1274.
32. David A. Morrow. Myocardial Infarction - A Companion to Braunwald’s Heart Disease. 20thEdition. Philadelphia: Elsevier. 2017.
33. Mengmeng Li1, Man Rao1, Kai Chen, Jianye Zhou, Jiangping Song. Selection of reference genes for gene expression studies in heart failure for left and right ventricles. Gene.2017; 620: 30-35.
34. Vavouranakis I, Lambrogiannakis E, Markakis G, Dermitzakis A, Haroniti Z, Ninidaki C, et al. Effect of home-based intervention on hospital readmission and quality of life in middle-aged patients with severe congestive heart failure: a 12-month Follow up study. Eur J Cardiovasc Nurs. 2003; 2 (2): 105-111.
35. Kurose S, Iwasaka J, Tsutsumi H, Yamanaka Y, Shinno H, and et al. Effect of exercise-based cardiac rehabilitation on non-culprit mild coronary plaques in the culprit coronary artery of patients with acute coronary syndrome. Heart Vessels. Heart Vessels. 2016; 31(6): 846-854.
36. Kwan G and Balady GJ. Cardiac rehabilitation 2012: advancing the fi eld through emerging science. Circulation 2012; 125: 369–373.
37. Perk J, De Backer G, Gohlke H, and et al. European guidelines on cardiovascular disease prevention in clinical practice (version 2012). the fi fth joint task force of the European society of cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of nine societies and by invited experts). Eur Heart J. 2012; 33(13): 1635-1701.
38. Thandavarayan RA, Watanabe K, Ma M, Veeraveedu PT, Gurusamy N, Palaniyandi SS, and et al. 14-3-3 protein regulates Ask1 signaling and protects against diabetic cardiomyopathy. Biochem Pharmacol. 2008; 75(9): 1797–1806.

38. Thandavarayan RA, Watanabe K, Ma M, Veeraveedu PT, Gurusamy N, Palaniyandi SS, and et al. 14-3-3 protein regulates Ask1 signaling and protects against diabetic cardiomyopathy. Biochem Pharmacol. 2008; 75(9): 1797–1806.
39. Nairi khob H.R. The effect of 8 weeks of resistance training on modifying sd LDL and galactine-3 changes due to an intense power of exercise session. [MSc]. Shiraz: Islamic Azad university; 1395.
40. Khaje Yian N. The effect of 8 weeks of endurance training on modifying sd LDL and galactine-3 changes due to an intense endurance of exercise session. [MSc]. Shiraz: Islamic Azad university; 1395.
41. Hashemi Z, Moghadasi M. Comparison of Galectin-3 and NT-ProBNP levels in strength and endurance elite athletes. Metabolism and Exercise A bioannual journal. 1395; 6(1): 49-57.
42. Naraghi S. The effect of a circular resistance training session on changes in NTproBNP and galactine-3 non-athletic men. [MSc]. Shiraz: Islamic Azad university; 1395.
43. Ghasami M. The effect of an exhausting aerobic Exercise session on NTproBNP and Galactine-3 changes in non-athlete men. [MSc]. Shiraz: Islamic Azad university; 1395.

44. Farzanegi P, Samiee M, Sabbaghian Z. Interactive effect of regular aerobic training and milk consumption on some inflammatory markers and lipid profi le in overweight boys. Koomesh. 1395; 17 (3): 627-635.
45. Song X, Qian X, Shen M, Jiang R, Wagner MB, Ding G, and et al. Protein kinase C promotes cardiac fi brosis and heart failure by modulating galectin-3 expression. Biochim Biophys Acta. 2015; 1853(2): 513-521.
46. Sharma U, Rhaleb NE, Pokharel S, Harding P, Rasoul S, Peng H, and et al. Novel anti-inflammatory mechanisms of N-Acetyl-SerAsp-Lys-Pro in hypertension induced target organ damage. Am J Physiol. 2008; 294(3): 1226–1232.