دوره 19، شماره 22 - ( 10-1400 )
جلد 19 شماره 22 صفحات 54-37 |
برگشت به فهرست نسخه ها
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
alabaf yousefi F, pouzesh jadidi R, Bashiri J, Vakili J. Effects of HIIT and Curcumin Supplementation on Rat Cardiac Fibrosis Signaling Pathway Following Myocardial Infraction. RSMT 2021; 19 (22) :37-54
URL: http://jsmt.khu.ac.ir/article-1-477-fa.html
URL: http://jsmt.khu.ac.ir/article-1-477-fa.html
اعلاباف یوسفی فریده، پوزش جدیدی رقیه، بشیری جبار، آزالی علمداری کریم، وکیلی جواد. اثرات تمرین تناوبی شدید و مکمل کورکومین بر پیام‌رسانی مسیر فیبروز قلبی موش‌های صحرایی متعاقب سکته قلبی. پژوهش در طب ورزشی و فناوری. 1400; 19 (22) :37-54
دانشگاه آزاد اسلامی تبریز ، Poozesh@iaut.ac.ir
چکیده: (3172 مشاهده)
هدف: هدف تحقیق تأثیر 12 هفته تمرین تناوبی شدید (HIIT) به همراه مصرف کورکومین بر مقدار بیان FSTL1، Smad7 و کلاژن‌های نوع I، III و IV بطن چپ موش‌های صحرایی نر مدل سکته قلبی بود. روش‌شناسی: پس از القای سکته قلبی، 48 سر موش صحرائی به پنج گروه: مرجع، تمرین، کورکومین، توأم (تمرین+کورکومین) و کنترل تقسیم شدند. پس از کشتار گروه مرجع برای تأیید بروز سکته، کورکومین روزانه 15 میلی‌گرم به ازای هر کیلوگرم وزن بدن به صورت گاواژ استفاده شد. جلسات تمرین HIIT پنج روز در هفته، هر جلسه شامل 60 دقیقه متشکل از 10 وهله (هر وهله چهار دقیقه) دویدن با شدت 90-85 درصد از vVO2 peak با دو دقیقه فاصله استراحت فعال در بین تکرارهای دویدن با شدت 50-45 درصد از vVO2 peak برگزار شدند. مقدار بیان پروتئین‌های FSTL1، Smad7 و همچنین کلاژن‌های I، III و IV بافت بطن چپ توسط وسترن بلات اندازه‌گیری شدند. یافته‌ها: پس از هر سه مداخله شامل تمرین، کورکومین و توأم، وزن قلب به‌طور معنی‌داری بیشتر (به ترتیب 001/0=P، 018/0=P و 001/0=P) و مقدار بیان کلاژن نوع IV کمتر (001/0=P در هر سه مورد) از گروه کنترل بودند. فقط در گروه توأم مقدار بیان کلاژن نوع III قلب به‌طور معنی‌داری کمتر (033/0=P) و FSTL و Smad7 (001/0=P) و Smad7 (008/0=P) بیشتر از گروه کنترل بود. نتیجه‌گیری: کاهش کلاژن نوع IV بدون مرگ‌ومیر در اثر اعمال هر سه مداخله، شاید به ایمن بودن تمرین HIIT و مکمل کورکومین برای کاهش روند فیبروز قلبی متعاقب سکته دلالت کند؛ اما فقط مداخله توأم سبب کاهش بیان پروتئین کلاژن نوع III و افزایش FSTL و Smad7 در بطن چپ دچار سکته شد که زمینه تجویز توأم کورکومین و HIIT برای کسب نتایج بهتر را فراهم می‌کند؛ اما به دلیل محدودیت‌های تحقیق و کمبود شواهد انسانی، همچنان نیاز به تحقیقات بیشتر باقی است.
نوع مطالعه: پژوهشي |
موضوع مقاله:
فیزیولوژی ورزشی
دریافت: 1399/12/5 | پذیرش: 1400/5/25 | انتشار: 1400/10/1
دریافت: 1399/12/5 | پذیرش: 1400/5/25 | انتشار: 1400/10/1
فهرست منابع
1. Mokhtari‐Zaer, A., Marefati, N., Atkin, SL., Butler, AE, Sahebkar, A. (2019). The protective role of curcumin in myocardial ischemia-reperfusion injury. Journal of Cellular Physiology. 234(1):214-22. [DOI:10.1002/jcp.26848]
2. Garza, MA., Wason, EA, Zhang, JQ. (2015). Cardiac remodeling and physical training post myocardial infarction. World Journal of Cardiology. 7(2):52-64. [DOI:10.4330/wjc.v7.i2.52]
3. Ghahramani, M., Kaikhosro Doulatyari, P, Rouzbahani, M. (2021). Investigation Effect of Exercise and Physical Activity on Cardiac Troponins: A Systematic Review. Journal of Applied Health Studies in Sport Physiology. 8(1):1-10. (Persian)
4. Fernández-Hernando, C., Ackah, E., Yu, J., Suárez, Y., Murata, T., Iwakiri, Y, et al. (2007). Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease. Cell Metabolism. 6(6):446-57. [DOI:10.1016/j.cmet.2007.10.007]
5. Karam, R., Healy, BP, Wicker, P. (1990). Coronary reserve is depressed in postmyocardial infarction reactive cardiac hypertrophy. Circulation. 81(1):238-46. [DOI:10.1161/01.CIR.81.1.238]
6. Shiojima, I. (2005). Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. Journal of Clinical Investigation. 115(8):2108-18. [DOI:10.1172/JCI24682]
7. Lara-Pezzi, E., Felkin, LE., Birks, EJ., Sarathchandra, P., Panse, KD., George, R, et al. (2008). Expression of Follistatin-Related Genes Is Altered in Heart Failure. Endocrinology. 149(11):5822-7. [DOI:10.1210/en.2008-0151]
8. Ouchi, N., Oshima, Y., Ohashi, K., Higuchi, A., Ikegami, C., Izumiya, Y, et al. (2008). Follistatin-like 1, a Secreted Muscle Protein, Promotes Endothelial Cell Function and Revascularization in Ischemic Tissue through a Nitric-oxide Synthase-dependent Mechanism. Journal of Biological Chemistry. 283(47):32802-11. [DOI:10.1074/jbc.M803440200]
9. El-Armouche, A., Ouchi, N., Tanaka, K., Doros, G., Wittköpper, K., Schulze, T, et al. (2011). Follistatin-like 1 in chronic systolic heart failure: a marker of left ventricular remodeling. Circulation: Heart Failure. 4(5):621-7. [DOI:10.1161/CIRCHEARTFAILURE.110.960625]
10. Shimano, M., Ouchi, N., Nakamura, K., van Wijk, B., Ohashi, K., Asaumi, Y, et al. (2011). Cardiac myocyte follistatin-like 1 functions to attenuate hypertrophy following pressure overload. Proceedings of the National Academy of Sciences. 108(43):E899-E906. [DOI:10.1073/pnas.1108559108]
11. Xi, Y., Hao, M, Tian, Z. (2019). Resistance Exercise Increases the Regulation of Skeletal Muscle FSTL1 Consequently Improving Cardiac Angiogenesis in Rats with Myocardial Infarctions. Journal of Science in Sport and Exercise.1-10. [DOI:10.1007/s42978-019-0009-4]
12. Eulertaimor, G, Heger, J. (2006). The complex pattern of SMAD signaling in the cardiovascular system☆. Cardiovascular Research. 69(1):15-25. [DOI:10.1016/j.cardiores.2005.07.007]
13. Yuan, S-M, Jing, H. (2010). Cardiac pathologies in relation to Smad-dependent pathways. Interactive CardioVascular and Thoracic Surgery. 11(4):455-60. [DOI:10.1510/icvts.2010.234773]
14. Sakata, Y., Chancey, AL., Divakaran, VG., Sekiguchi, K., Sivasubramanian, N, Mann, DL. (2007). Transforming growth factor-β receptor antagonism attenuates myocardial fibrosis in mice with cardiac-restricted overexpression of tumor necrosis factor. Basic Research in Cardiology. 103(1):60-8. [DOI:10.1007/s00395-007-0689-5]
15. Tessone, A., Feinberg, MS., Barbash, IM., Reich, R., Holbova, R., Richmann, M, et al. (2005). Effect of Matrix Metalloproteinase Inhibition by Doxycycline on Myocardial Healing and Remodeling after Myocardial Infarction. Cardiovascular Drugs and Therapy. 19(6):383-90. [DOI:10.1007/s10557-005-5201-6]
16. Spinale, FG., Gunasinghe, H., Sprunger, PD., Baskin, JM, Bradham, WC. (2002). Extracellular degradative pathways in myocardial remodeling and progression to heart failure. Journal of Cardiac Failure. 8(6):S332-S8. [DOI:10.1054/jcaf.2002.129259]
17. Cleutjens, JPM., Smits, JFM, Daemen, MJAP. (1992). Type I and III collagen mRNA and protein increase in the infarcted and non-infarcted rat heart after myocardial infarction. Journal of Molecular and Cellular Cardiology. 24:S50. [DOI:10.1016/0022-2828(92)91651-K]
18. Brown, RD., Ambler, SK., Mitchell, MD, Long, CS. (2005). THE CARDIAC FIBROBLAST: Therapeutic Target in Myocardial Remodeling and Failure. Annual Review of Pharmacology and Toxicology. 45(1):657-87. [DOI:10.1146/annurev.pharmtox.45.120403.095802]
19. Sun, Y. (2008). Myocardial repair/remodelling following infarction: roles of local factors. Cardiovascular Research. 81(3):482-90. [DOI:10.1093/cvr/cvn333]
20. Wang, N-P., Wang, Z-F., Tootle, S., Philip, T, Zhao, Z-Q. (2012). Curcumin promotes cardiac repair and ameliorates cardiac dysfunction following myocardial infarction. British Journal of Pharmacology. 167(7):1550-62. [DOI:10.1111/j.1476-5381.2012.02109.x]
21. Ma, J., Ma, SY, Ding, CH. (2017). Curcumin reduces cardiac fibrosis by inhibiting myofibroblast differentiation and decreasing transforming growth factor beta1 and matrix metalloproteinase 9 / tissue inhibitor of metalloproteinase 1. Chinese Journal of Integrative Medicine. 23(5):362-9. [DOI:10.1007/s11655-015-2159-5]
22. Xiao, J., Sheng, X., Zhang, X., Guo, M, Ji, X. (2016). Curcumin protects against myocardial infarction-induced cardiac fibrosis via SIRT1 activation in vivo and in vitro. Drug Design, Development and Therapy. 10:1267. [DOI:10.2147/DDDT.S104925]
23. Ma, J., Ma, S-y, Ding, C-h. (2017). Curcumin reduces cardiac fibrosis by inhibiting myofibroblast differentiation and decreasing transforming growth factor β1 and matrix metalloproteinase 9/tissue inhibitor of metalloproteinase 1. Chinese Journal of Integrative Medicine. 23(5):362-9. [DOI:10.1007/s11655-015-2159-5]
24. Whitham, M., Parker, BL., Friedrichsen, M., Hingst, JR., Hjorth, M., Hughes, WE, et al. (2018). Extracellular vesicles provide a means for tissue crosstalk during exercise. Cell Metabolism. 27(1):237-51. e4. [DOI:10.1016/j.cmet.2017.12.001]
25. Bei, Y., Xu, T., Lv, D., Yu, P., Xu, J., Che, L, et al. (2017). Exercise-induced circulating extracellular vesicles protect against cardiac ischemia-reperfusion injury. Basic Research in Cardiology. 112(38):1-15. [DOI:10.1007/s00395-017-0628-z]
26. Choi, H-Y., Han, H-J., Choi, J-w., Jung, H-Y, Joa, K-L. (2018). Superior effects of high-intensity interval training compared to conventional therapy on cardiovascular and psychological aspects in myocardial infarction. Annals of Rehabilitation Medicine. 42(1):145-53. [DOI:10.5535/arm.2018.42.1.145]
27. Hannan, AL., Hing, W., Simas, V., Climstein, M., Coombes, JS., Jayasinghe, R, et al. (2018). High-intensity interval training versus moderate-intensity continuous training within cardiac rehabilitation: a systematic review and meta-analysis. Open Access Journal Sports Medicine. 9:1-17. [DOI:10.2147/OAJSM.S150596]
28. Ebadi, B., Damirchi, A., Alamdari, KA., Darbandi-Azar, A, Naderi, N. (2018). Cardiomyocyte mitochondrial dynamics in health and disease and the role of exercise training: A brief review. Research in Cardiovascular Medicine. 7(3):107-15. [DOI:10.4103/rcm.rcm_11_18]
29. Jeremic, N., Weber, GJ., Theilen, NT, Tyagi, SC. (2020). Cardioprotective effects of high‐intensity interval training are mediated through microRNA regulation of mitochondrial and oxidative stress pathways. Journal of Cellular Physiology. 235(6):5229-40. [DOI:10.1002/jcp.29409]
30. Moieni, A, Hosseini, SA. (2020). Effect of Resistance Training Combined with Curcumin Supplementation on Expression of Regulatory Genes Related to Myocardial Remodeling in Obese Rats. Journal of Applied Health Studies in Sport Physiology. 7(2):45-52. (Persian)
31. Liao, Z., Li, D., Chen, Y., Li, Y., Huang, R., Zhu, K, et al. (2019). Early moderate exercise benefits myocardial infarction healing via improvement of inflammation and ventricular remodelling in rats. Journal of Cellular and Molecular Medicine. 23(12):8328-42. [DOI:10.1111/jcmm.14710]
32. Wang, B., Zhou, R., Wang, Y., Liu, X., Shou, X., Yang, Y, et al. (2020). Effect of high-intensity interval training on cardiac structure and function in rats with acute myocardial infarct. Biomedicine & Pharmacotherapy. 131:110690. [DOI:10.1016/j.biopha.2020.110690]
33. Rodrigues, B., Figueroa, DM., Mostarda, CT., Heeren, MV., Irigoyen, M-C, De Angelis, KJCd. (2007). Maximal exercise test is a useful method for physical capacity and oxygen consumption determination in streptozotocin-diabetic rats. Cardiovascular Diabetology. 6(38):1-10. [DOI:10.1186/1475-2840-6-38]
34. Hafstad, AD., Lund, J., Hadler-Olsen, E., Höper, AC., Larsen, TS, Aasum, E. (2013). High-and moderate-intensity training normalizes ventricular function and mechanoenergetics in mice with diet-induced obesity. Diabetes. 62(7):2287-94. [DOI:10.2337/db12-1580]
35. Biswas, J., Roy, S., Mukherjee, S., Sinha, D, Roy, MJAPjocpA. (2010). Indian spice curcumin may be an effective strategy to combat the genotoxicity of arsenic in Swiss albino mice. 11(1):239-47.
36. Shen, H., Cui, G., Li, Y., Ye, W., Sun, Y., Zhang, Z, et al. (2019). Follistatin-like 1 protects mesenchymal stem cells from hypoxic damage and enhances their therapeutic efficacy in a mouse myocardial infarction model. Stem Cell Research & Therapy. 10(1):17. [DOI:10.1186/s13287-018-1111-y]
37. Kon, M., Ebi, Y, Nakagaki, K. (2019). Effects of acute sprint interval exercise on follistatin-like 1 and apelin secretions. Archives of Physiology and Biochemistry.1-5. [DOI:10.1080/13813455.2019.1628067]
38. Xi, Y., Gong, D-W, Tian, Z. (2016). FSTL1 as a potential mediator of exercise-induced cardioprotection in post-myocardial infarction rats. Scientific reports. 6(1):1-11. [DOI:10.1038/srep32424]
39. Wei, K., Serpooshan, V., Hurtado, C., Diez-Cunado, M., Zhao, M., Maruyama, S, et al. (2015). Epicardial FSTL1 reconstitution regenerates the adult mammalian heart. Nature. 525(7570):479-85. [DOI:10.1038/nature15372]
40. Wang, S-Q., Li, D, Yuan, Y. (2019). Long-term moderate intensity exercise alleviates myocardial fibrosis in type 2 diabetic rats via inhibitions of oxidative stress and TGF-β1/Smad pathway. The Journal of Physiological Sciences. 69(6):861-73. [DOI:10.1007/s12576-019-00696-3]
41. Schreckenberg, R., Horn, A-M., da Costa Rebelo, RM., Simsekyilmaz, S., Niemann, B., Li, L, et al. (2017). Effects of 6-months' Exercise on Cardiac Function, Structure and Metabolism in Female Hypertensive Rats-The Decisive Role of Lysyl Oxidase and Collagen III. Frontiers in Physiology. 8(556):1-11. [DOI:10.3389/fphys.2017.00556]
42. Rodríguez, C., Martínez-González, J., Raposo, B., Alcudia, JF., Guadall, A, Badimon, L. (2008). Regulation of lysyl oxidase in vascular cells: lysyl oxidase as a new player in cardiovascular diseases. Cardiovascular Research. 79(1):7-13. [DOI:10.1093/cvr/cvn102]
43. López, B., González, A., Hermida, N., Valencia, F., de Teresa, E, Díez, J. (2010). Role of lysyl oxidase in myocardial fibrosis: from basic science to clinical aspects. American Journal of Physiology-Heart and Circulatory Physiology. 299(1):H1-H9. [DOI:10.1152/ajpheart.00335.2010]
44. Giampuzzi, M., Botti, G., Di Duca, M., Arata, L., Ghiggeri, G., Gusmano, R, et al. (2000). Lysyl oxidase activates the transcription activity of human collagene iii promoter possible involvement of ku antigen. Journal of Biological Chemistry. 275(46):36341-9. [DOI:10.1074/jbc.M003362200]
45. de Souza, RR. (2002). Aging of myocardial collagen. Biogerontology. 3(6):325-35. [DOI:10.1023/A:1021312027486]
46. Watanabe, T., Kusachi, S., Yamanishi, A., Kumashiro, H., Nunoyama, H., Sano, I, et al. (1998). Localization of Type IV Collagen α Chain in the Myocardium of Dilated and Hypertrophic Cardiomyopathy. Japanese Heart Journal. 39(6):753-62. [DOI:10.1536/ihj.39.753]
47. Nielsen, SH., Mouton, AJ., DeLeon-Pennell, KY., Genovese, F., Karsdal, M, Lindsey, ML. (2019). Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes. Matrix Biology. 75-76:43-57. [DOI:10.1016/j.matbio.2017.12.001]
48. Varga, I., Kyselovič, J., Galfiova, P, Danisovic, L. The Non-cardiomyocyte Cells of the Heart. Their Possible Roles in Exercise-Induced Cardiac Regeneration and Remodeling. In: Xiao J, editor. Exercise for Cardiovascular Disease Prevention and Treatment: From Molecular to Clinical, Part 1. 999. Singapore: Springer Singapore; 2017. p. 117-36. [DOI:10.1007/978-981-10-4307-9_8]
49. Zhou, D., Hao, D., Wei, L., Zhang, T., Weimin, L., Zhang, X, et al. (2017). Effect of aerobics exercise on myocardial fibrosis after acute myocardial infarction in rat. Journal of Chinese Physician. 19(6):852-4.
50. de Freitas, JS., Neves, CA., Del Carlo, RJ., Belfort, FG., Lavorato, VN., Silame-Gomes, LHL, et al. (2019). Effects of exercise training and stem cell therapy on the left ventricle of infarcted rats. Revista Portuguesa de Cardiologia (English Edition). 38(9):649-56. [DOI:10.1016/j.repce.2019.02.014]
51. Szabó, R., Karácsonyi, Z., Börzsei, D., Juhász, B., Al-Awar, A., Török, S, et al. (2018). Role of exercise-induced cardiac remodeling in ovariectomized female rats. Oxidative Medicine and Cellular Longevity. 2018:6709742. [DOI:10.1155/2018/6709742]
52. Amani, M., Jeddi, S., Ahmadiasl, N., Usefzade, N, Zaman, J. (2013). Effect of HEMADO on Level of CK-MB and LDH Enzymes after Ischemia/Reperfusion Injury in Isolated Rat Heart. Bioimpacts. 3(2):101-4.
53. Yang, Z., Berr, SS., Gilson, WD., Toufektsian, M-C, French, BA. (2004). Simultaneous evaluation of infarct size and cardiac function in intact mice by contrast-enhanced cardiac magnetic resonance imaging reveals contractile dysfunction in noninfarcted regions early after myocardial infarction. Circulation. 109(9):1161-7. [DOI:10.1161/01.CIR.0000118495.88442.32]
54. Nirmala, C, Puvanakrishnan, R. (1996). Protective role of curcumin against isoproterenol induced myocardial infarction in rats. Molecular and Cellular Biochemistry. 159(2):85-93. [DOI:10.1007/BF00420910]
55. Boarescu, P-M., Chirilă, I., Bulboacă, AE., Bocșan, IC., Pop, RM., Gheban, D, et al. (2019). Effects of curcumin nanoparticles in isoproterenol-induced myocardial infarction. Oxidative Medicine and Cellular Longevity. 2019. 7847142. [DOI:10.1155/2019/7847142]
ارسال پیام به نویسنده مسئول
| بازنشر اطلاعات | |
 |
این مقاله تحت شرایط Creative Commons Attribution-NonCommercial 4.0 International License قابل بازنشر است. |
