تعداد نشریات | 29 |
تعداد شمارهها | 431 |
تعداد مقالات | 4,216 |
تعداد مشاهده مقاله | 6,797,033 |
تعداد دریافت فایل اصل مقاله | 5,044,043 |
آثار شدت تمرینات تناوبی بر پروتئینهای مرتبط با دینامیک میتوکندری در قلب رتهای نر مبتلابه انفارکتوس میوکارد | ||
پژوهشنامه فیزیولوژی ورزشی کاربردی | ||
مقاله 12، دوره 14، شماره 28، بهمن 1397، صفحه 159-172 اصل مقاله (278.27 K) | ||
نوع مقاله: مقاله پژوهشی | ||
شناسه دیجیتال (DOI): 10.22080/jaep.2019.13561.1718 | ||
نویسندگان | ||
ارسلان دمیرچی1؛ بابک عبادی* 2 | ||
1استاد فیزیولوژی ورزشی دانشکده علوم ورزشی دانشگاه گیلان، رشت، ایران | ||
2دانشجوی دکتری فیزیولوژی ورزش دانشکده تربیت بدنی و علوم ورزشی دانشگاه گیلان | ||
تاریخ دریافت: 10 بهمن 1396، تاریخ بازنگری: 05 اسفند 1396، تاریخ پذیرش: 23 اسفند 1396 | ||
چکیده | ||
مقدمه و هدف: انفارکتوس میوکارد (MI) شایعترین نوع بیماری قلبی می باشد. بر اساس مطالعات اخیر، اختلال در عملکرد میتوکندری در پیشرفت نارساییهای قلبی پذیرفتهشده است. فعالیت ورزشی نقش محافظتی در برابر بیماریهای قلبی عروقی دارد با این حال نقش پروتئینهای درگیر در داینامیک میتوکندری در پاسخ به فعالیت ورزشی بهخوبی مشخص نشده است. بنابراین، هدف پژوهش حاضر بررسی آثار شدت تمرینات تناوبی بر پروتئینهای مرتبط با داینامیک میتوکندری در قلب رتهای نر مبتلابه انفارکتوس میوکارد میباشد. موارد و روش ها: پژوهش حاضر، تجربی با طرح پسآزمون با گروه کنترل در رتهای ویستار 16 هفتهای بود. در این مطالعه، پس از ایجاد MI با بستن شریان کرونری(LAD) و اطمینان از ایجاد MI توسط اکوکاردیوگرافی، رتهای به گروههای تمرینی تناوبی باشدت بالا (HIIT)، متوسط (MIIT)، پایین (LIIT)، انفارکتوس میوکارد بیتمرین (MI-SED) و کنترل سالم (C) تقسیم شدند. 6 هفته پس از اجرای تمرینات ورزشی(5 جلسه در هفته، هرجلسه یک ساعت)، سطوح پروتئینهای MFN2، DRP1 و PGC-1α بافت قلب به روش وسترن بلات اندازهگیریوتحلیل دادهها با استفاده از آزمون ANOVA و تست تعقیبی بونفرونی در سطح معنی داری 05/0P≤ انجام شد. یافته ها: نتایج تحلیل داده ها نشان داد که سطوح پروتئین های MFN2 و PGC-1α در گروه MI-SED نسبت به کنترل سالم کاهش و سطوح پروتئنی DRP1 افزایش معنیداری داشت (05/0P≤). همچنین، سطوح پروتئینهای MFN2 و PGC-1α تنها در گروه MIIT نسبت به گروه MI-SED افزایش معنی داری داشت (05/0P≤) و بین سایر گروهها تفاوت معنی دار وجود نداشت (05/0P≤). با اینحال کاهش سطوح پروتئینی DRP1 در تمامی گروههای تمرینی نسبت به MI-SED معنیداری بود (05/0P≤) ولی تفاوتی بین سه شدت مختلف تمرین وجود نداشت (05/0P≤). نتیجه گیری: تمرین تناوبی با شدت متوسط (MIIT) منجر به بهبود پروتئینهای همجوشی و شکافت میتوکندری در رتهای مبتلا به انفارکتوس میوکارد میشود.در حالیکه تمرین تناوبی با شدت بالا و پایین (HIIT،LIIT) علی رغم کاهش معنی دار DRP-1، منجر به نغییرات قابل توجهی در محتوی پروتئینی MFN2 و PGC-1α نشد. | ||
کلیدواژهها | ||
انفارکتوس میوکارد؛ تمرین تناوبی؛ شدت فعالیت ورزشی؛ DRP1؛ MFN2T؛ PGC-1α؛ MFN2 | ||
عنوان مقاله [English] | ||
The effects of the intensity of interval training on mitochondrial dynamics-related proteins in the heart of male rats with myocardial infarction | ||
نویسندگان [English] | ||
Arsalan Damirchi1؛ Babak Ebadi2 | ||
1. | ||
2Cardiovascular Exercise Physiology Department, Faculty of Exercise Science, University of Guilan, Iran. | ||
چکیده [English] | ||
Introduction and Purpose: Myocardial infarction (MI) is the most common type of heart disease. According to recent studies, mitochondrial dysfunction has been accepted in the development of heart failure. Exercise training plays a protective role against cardiovascular disease. However, the role of proteins involved in mitochondrial dynamics is not understood in response to exercise training. Therefore, the aim of the present study was to investigate the effects of the intensity of interval training on mitochondrial dynamic proteins in the heart of male rats with myocardial infarction. Materials and Methods: The present study was performed with experimental posttest design method with control group in 16 week wistar rats. In this study, after MI with ligation of the left anterior descending coronary artery (LAD) and ensuring the creation of MI by echocardiography, rats were subjected to HIIT, MIIT and (LIIT training, Sham (MI-SED) and control (C). Six weeks after exercise, the levels of MFN2, DRP1 and PGC-1α proteins were measured by western blot . Results: data analysis showed that proteins level of MFN2 and PGC-1α decreased significantly in MI-SED group compared to healthy control and DRP1 protein levels increased significantly (P≤0.05). Also, MFN2 and PGC-1α proteins increased in MIIT compared with MI-SED and DRP1 protein levels decreased as well (P≤0.05). Discussion and conclusion: Moderate-intensity interval training (MIIT) leads to improved mitochondrial fusion and fusion proteins in rats with myocardial infarction. While high and low intensity interval training, despite increasing MFN2 and PGC-1α and reducing DRP1, failed to improve fusion and mitochondrial fission. | ||
کلیدواژهها [English] | ||
Myocardial Infarction, interval Training, Exercise Intensity, DRP1, MFN2T, PGC-1α, MFN2 | ||
مراجع | ||
##Vega-Lugo JA, Parodi-Rullán RM, Soto-Prado J, Chapa-Dubocq X, Javadov S (2017). The effects of myocardial infarction with or without subsequent reperfusion on respiratory function of mitochondria in rat heart. The FASEB Journal.;31(1 Supplement):1080.8-8.##Wu Y, Yin X, Wijaya C, Huang M-H, McConnell BK (2011). Acute myocardial infarction in rats. Journal of visualized experiments: JoVE. (48).##Lujan HL, DiCarlo SE (2013). Mimicking the endogenous current of injury improves post-infarct cardiac remodeling. Medical hypotheses.;81(4):521-3.##Zornoff LA, Paiva SA, Minicucci MF, Spadaro J (2009). Experimental myocardium infarction in rats: analysis of the model. Arquivos brasileiros de cardiologia.;93(4):434-40.##Cohn JN, Ferrari R, Sharpe N (2000). Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. Journal of the American College of Cardiology.;35(3):569-82.##Heather LC, Carr CA, Stuckey DJ, Pope S, Morten KJ, Carter EE, et al (2009). Critical role of complex III in the early metabolic changes following myocardial infarction. Cardiovascular research.;85(1):127-36.##Sena S, Hu P, Zhang D, Wang X, Wayment B, Olsen C, et al (2009). Impaired insulin signaling accelerates cardiac mitochondrial dysfunction after myocardial infarction. Journal of molecular and cellular cardiology.;46(6):910-8.##Tsutsui H, Kinugawa S, Matsushima S (2008). Mitochondrial oxidative stress and dysfunction in myocardial remodelling. Cardiovascular research.;81(3):449-56.##Rosca MG, Vazquez EJ, Kerner J, Parland W, Chandler MP, Stanley W, et al (2008). Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation. Cardiovascular research.;80(1):30-9.##Hausenloy DJ, Yellon DM (2003). The mitochondrial permeability transition pore: its fundamental role in mediating cell death during ischaemia and reperfusion. Academic Press.##Halestrap AP (2009). Mitochondria and reperfusion injury of the heart—a holey death but not beyond salvation. Journal of bioenergetics and biomembranes.;41(2):113-21.##Zhou S, Sun W, Zhang Z, Zheng Y (2014). The role of Nrf2-mediated pathway in cardiac remodeling and heart failure. Oxidative medicine and cellular longevity.##Hori M, Nishida K (2008). Oxidative stress and left ventricular remodelling after myocardial infarction. Cardiovascular research.81(3):457-64.##Huss JM, Kelly DP (2005). Mitochondrial energy metabolism in heart failure: a question of balance. Journal of Clinical Investigation.;115(3):547.##Finck BN, Kelly DP (2007). Peroxisome proliferator–activated receptor γ coactivator-1 (PGC-1) regulatory cascade in cardiac physiology and disease. Circulation.115(19):2540-8.##Chan DC (2012). Fusion and fission: interlinked processes critical for mitochondrial health. Annual review of genetics.46:265-87.##Hall A, Burke N, Dongworth R, Hausenloy D (2014). Mitochondrial fusion and fission proteins: novel therapeutic targets for combating cardiovascular disease. British journal of pharmacology. 171(8):1890-906.##Iglewski M, Hill JA, Lavandero S, Rothermel BA (2010). Mitochondrial fission and autophagy in the normal and diseased heart. Current hypertension reports.12(6):418-25.##Ong S-B, Hausenloy DJ (2010). Mitochondrial morphology and cardiovascular disease. Cardiovascular research.88(1):16-29.##Disatnik M-H, Ferreira JC, Campos JC, Gomes KS, Dourado PM, Qi X, et al (2013). Acute inhibition of excessive mitochondrial fission after myocardial infarction prevents long-term cardiac dysfunction. Journal of the American Heart Association.2(5):e000461.## Jiang H-K, Wang Y-H, Sun L, He X, Zhao M, Feng Z-H, et al (2014). Aerobic interval training attenuates mitochondrial dysfunction in rats post-myocardial infarction: roles of mitochondrial network dynamics. International journal of molecular sciences.15(4):5304-22.##Icks A, Claessen H, Kirchberger I, Heier M, Peters A, Trentinaglia I, et al (2014). Mortality after first myocardial infarction in diabetic and non-diabetic people between 1985 and 2009. The MONICA/KORA registry. European journal of epidemiology.29(12):899-909.##Hosseini SH, Ghaemian A, Mehdizadeh E, Ashraf H (2014). Levels of anxiety and depression as predictors of mortality following myocardial infarction: A 5-year follow-up. Cardiology journal.21(4):370-7.##Ellison GM, Waring CD, Vicinanza C, Torella D (2012). Physiological cardiac remodelling in response to endurance exercise training: cellular and molecular mechanisms. Heart.98(1):5-10.##Weiner RB, Baggish AL (2012). Exercise-induced cardiac remodeling. Progress in cardiovascular diseases.54(5):380-6.##Lee Y, Min K, Talbert EE, Kavazis AN, Smuder AJ, Willis WT, et al (2012). Exercise protects cardiac mitochondria against ischemia–reperfusion injury. Medicine & Science in Sports & Exercise.44(3):397-405.##Quindry JC, Miller L, McGinnis G, Kliszczewicz B, Irwin JM, Landram M, et al (2012). Ischemia reperfusion injury, K ATP channels, and exercise-induced cardioprotection against apoptosis. Journal of Applied Physiology.113(3):498-506.##Yan Z, Lira VA, Greene NP (2012). Exercise training-induced regulation of mitochondrial quality. Exercise and sport sciences reviews.40(3):159.##Cartoni R, Léger B, Hock MB, Praz M, Crettenand A, Pich S, et al (2005). Mitofusins 1/2 and ERRα expression are increased in human skeletal muscle after physical exercise. The Journal of physiology.567(1):349-58.##Perry CG, Lally J, Holloway GP, Heigenhauser GJ, Bonen A, Spriet LL (2010). Repeated transient mRNA bursts precede increases in transcriptional and mitochondrial proteins during training in human skeletal muscle. The Journal of physiology.;588(23):4795-810.##Kuzmicic J, del Campo A, López-Crisosto C, Morales PE, Pennanen C, Bravo-Sagua R, et al (2011). Mitochondrial dynamics: a potential new therapeutic target for heart failure. Revista Española de Cardiología (English Edition).64(10):916-23.##Finck BN, Kelly DP (2006). PGC-1 coactivators: inducible regulators of energy metabolism in health and disease. Journal of Clinical Investigation.116(3):615.##Huh JY, Mougios V, Kabasakalis A, Fatouros I, Siopi A, Douroudos II, et al (2014). Exercise-induced irisin secretion is independent of age or fitness level and increased irisin may directly modulate muscle metabolism through AMPK activation. The Journal of Clinical Endocrinology & Metabolism.99(11):E2154-E61.##Fukuda S, Kaga S, Sasaki H, Zhan L, Zhu L, Otani H, et al (2004). Angiogenic signal triggered by ischemic stress induces myocardial repair in rat during chronic infarction. Journal of molecular and cellular cardiology.36(4):547-59.##Samsamshariat SA, Samsamshariat ZA, Movahed M-R (2005). A novel method for safe and accurate left anterior descending coronary artery ligation for research in rats. Cardiovascular Revascularization Medicine.6(3):121-3.##Scherrer-Crosbie M, Thibault HB (2008). Echocardiography in translational research: of mice and men. Journal of the American Society of Echocardiography.21(10):1083-92.##Waring CD, Vicinanza C, Papalamprou A, Smith AJ, Purushothaman S, Goldspink DF, et al (2012). The adult heart responds to increased workload with physiologic hypertrophy, cardiac stem cell activation, and new myocyte formation. European heart journal.35(39):2722-31.##Kemi OJ, Haram PM, Loennechen JP, Osnes J-B, Skomedal T, Wisløff U, et al (2005). Moderate vs. high exercise intensity: differential effects on aerobic fitness, cardiomyocyte contractility, and endothelial function. Cardiovascular research.67(1):161-72.##Kraljevic J, Marinovic J, Pravdic D, Zubin P, Dujic Z, Wisloff U, et al (2013). Aerobic interval training attenuates remodelling and mitochondrial dysfunction in the post-infarction failing rat heart. Cardiovascular research.99(1):55-64.##Ong S-B, Subrayan S, Lim SY, Yellon DM, Davidson SM, Hausenloy DJ (2010). Inhibiting mitochondrial fission protects the heart against ischemia/reperfusion injury. Circulation.121(18):2012-22.##Din S, Mason M, Völkers M, Johnson B, Cottage CT, Wang Z, et al (2013). Pim-1 preserves mitochondrial morphology by inhibiting dynamin-related protein 1 translocation. Proceedings of the National Academy of Sciences.110(15):5969-74.##Leistner DM, Zeiher AM (2012). Novel avenues for cell therapy in acute myocardial infarction. Am Heart Assoc.##Yu T, Robotham JL, Yoon Y (2006). Increased production of reactive oxygen species in hyperglycemic conditions requires dynamic change of mitochondrial morphology. Proceedings of the National Academy of Sciences of the United States of America.103(8):2653-8.##Gomez-Lazaro M, Bonekamp NA, Galindo MF, Jordán J, Schrader M (2008). 6-Hydroxydopamine (6-OHDA) induces Drp1-dependent mitochondrial fragmentation in SH-SY5Y cells. Free Radical Biology and Medicine.44(11):1960-9.##Parker L, McGuckin TA, Leicht AS (2014). Influence of exercise intensity on systemic oxidative stress and antioxidant capacity. Clinical physiology and functional imaging.34(5):377-83.##St-Pierre J, Drori S, Uldry M, Silvaggi JM, Rhee J, Jäger S, et al (2006). Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. Cell;127(2):397-408.##Liesa M, Borda-d'Água B, Medina-Gómez G, Lelliott CJ, Paz JC, Rojo M, et al (2008). Mitochondrial fusion is increased by the nuclear coactivator PGC-1β. PloS one.3(10):e3613.##Ding H, Jiang N, Liu H, Liu X, Liu D, Zhao F, et al (2010). Response of mitochondrial fusion and fission protein gene expression to exercise in rat skeletal muscle. Biochimica et Biophysica Acta (BBA)-General Subjects.1800(3):250-6.##Kang C, O'moore KM, Dickman JR, Ji LL (2009). Exercise activation of muscle peroxisome proliferator-activated receptor-γ coactivator-1α signaling is redox sensitive. Free Radical Biology and Medicine.47(10):1394-400.## | ||
آمار تعداد مشاهده مقاله: 1,326 تعداد دریافت فایل اصل مقاله: 1,144 |