سه شنبه 6 آذر 1403
دوره 8، شماره 2 - ( 4-1397 )
جلد 8 شماره 2 صفحات 121-115 |
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:
Ghahremani R, Salehi I, Komaki A, Damirchi A. Preconditioning Effect of High-Intensity Aerobic Training on Myocardial Ischemia-Reperfusion Injury and Beclin-1 Gene Expression in Rats. PTJ 2018; 8 (2) :115-121
URL: http://ptj.uswr.ac.ir/article-1-364-fa.html
URL: http://ptj.uswr.ac.ir/article-1-364-fa.html
Preconditioning Effect of High-Intensity Aerobic Training on Myocardial Ischemia-Reperfusion Injury and Beclin-1 Gene Expression in Rats. فصلنامه فیزیک درمانی. 1397; 8 (2) :115-121
چکیده: (4251 مشاهده)
Purpose: Ischemia-Reperfusion (IR) injury is one of the most common cardiac disorders leading to irreversible heart damage. Many underlying mechanisms seem to be involved, among which disruption of cellular autophagy balance. Since physical training has a beneficial effect on the improvement of autophagy balance, it may have a cardioprotective effect against IR injury. This study investigates the protective role of aerobic training from cardiac IR injury and the autophagy process as a possible mechanism.
Methods: Thirty-two male Wistar rats (8 weeks old) were divided into control, sham, control plus IR, and training plus IR groups (8 rats each). The training group was exercised aerobically on a treadmill for 8 weeks (5 d/wk). After 8 weeks, the anesthetized rats underwent left thoracotomy (sham, control plus IR, and training plus IR groups) to access the left anterior descending coronary artery, which was occluded by a silk suture for 30 min and then released for 90 min of reperfusion (IR groups). Triphenyltetrazolium chloride staining was used to determine the infarct size. The gene expression of Beclin-1 was evaluated by real-time polymerase chain reaction. One-way ANOVA was used for statistical analysis with the significance level set at P≤0.05.
Results: The cardiac infarct size was smaller in training plus IR (20.24±5.7%) group compared to that in the control plus IR (35.9±2.3%) group (P≤0.05). On the other hand, IR operation significantly increased the gene expression of Beclin-1, while exercise training prevented expression of the mentioned gene in training plus IR group (P≤0.05).
Conclusion: Aerobic training can protect the heart against Ischemia-Reperfusion injury. It seems that improvement of autophagy balance during IR injury may be involved in exercise-induced cardioprotection against Ischemia-Reperfusion.
Methods: Thirty-two male Wistar rats (8 weeks old) were divided into control, sham, control plus IR, and training plus IR groups (8 rats each). The training group was exercised aerobically on a treadmill for 8 weeks (5 d/wk). After 8 weeks, the anesthetized rats underwent left thoracotomy (sham, control plus IR, and training plus IR groups) to access the left anterior descending coronary artery, which was occluded by a silk suture for 30 min and then released for 90 min of reperfusion (IR groups). Triphenyltetrazolium chloride staining was used to determine the infarct size. The gene expression of Beclin-1 was evaluated by real-time polymerase chain reaction. One-way ANOVA was used for statistical analysis with the significance level set at P≤0.05.
Results: The cardiac infarct size was smaller in training plus IR (20.24±5.7%) group compared to that in the control plus IR (35.9±2.3%) group (P≤0.05). On the other hand, IR operation significantly increased the gene expression of Beclin-1, while exercise training prevented expression of the mentioned gene in training plus IR group (P≤0.05).
Conclusion: Aerobic training can protect the heart against Ischemia-Reperfusion injury. It seems that improvement of autophagy balance during IR injury may be involved in exercise-induced cardioprotection against Ischemia-Reperfusion.
فهرست منابع
1. Dorweiler B, Pruefer D, Andrasi TB, Maksan SM, Schmiedt W, Neufang A, et al. Ischemia-Reperfusion injury. European Journal of Trauma and Emergency Surgery. 2007; 33(6):600-12. [DOI:10.1007/s00068-007-7152-z] [PMID] [DOI:10.1007/s00068-007-7152-z]
2. Hatmi ZN, Tahvildari S, Motlag AG, Kashani AS. Prevalence of coronary artery disease risk factors in Iran: A population based survey. BMC Cardiovascular Disorders. 2007; 7(1):32. [DOI:10.1186/1471-2261-7-32] [PMID] [PMCID]
3. Powers SK, Smuder AJ, Kavazis AN, Quindry JC. Mechanisms of exercise-induced cardioprotection. Physiology. 2014; 29(1):27-38. [DOI:10.1152/physiol.00030.2013] [PMID] [PMCID] [DOI:10.1152/physiol.00030.2013]
4. Lennon SL, Quindry JC, French JP, Kim S, Mehta JL, Powers SK. Exercise and myocardial tolerance to ischaemia‐reperfusion. Acta Physiologica Scandinavica. 2004; 182(2):161-9. [DOI:10.1111/j.1365-201X.2004.01346.x] [PMID] [DOI:10.1111/j.1365-201X.2004.01346.x]
5. Esposito F, Ronchi R, Milano G, Margonato V, Di Tullio S, Marini M, et al. Myocardial tolerance to ischemia–reperfusion injury, training intensity and cessation. European Journal of Applied Physiology. 2011; 111(5):859-68. [DOI:10.1007/s00421-010-1707-0] [PMID] [DOI:10.1007/s00421-010-1707-0]
6. Kavazis AN. Exercise preconditioning of the myocardium. Sports Medicine. 2009; 39(11):923-35. [DOI:10.2165/11317870-000000000-00000] [PMID] [DOI:10.2165/11317870-000000000-00000]
7. Tao L, Bei Y, Lin S, Zhang H, Zhou Y, Jiang J, et al. Exercise training protects against acute myocardial infarction via improving myocardial energy metabolism and mitochondrial biogenesis. Cellular Physiology and Biochemistry. 2015; 37(1):162-75. [DOI:10.1159/000430342] [PMID] [DOI:10.1159/000430342]
8. Ghahremani R, Damirchi A, Salehi I, Komaki A, Esposito F. Mitochondrial dynamics as an underlying mechanism involved in aerobic exercise training-induced cardioprotection against Ischemia-Reperfusion injury. Life Sciences. 2018; 213:102-8. [DOI:10.1016/j.lfs.2018.10.035] [PMID] [DOI:10.1016/j.lfs.2018.10.035]
9. Wu JJ, Quijano C, Chen E, Liu H, Cao L, Fergusson MM, et al. Mitochondrial dysfunction and oxidative stress mediate the physiological impairment induced by the disruption of autophagy. Aging. 2009; 1(4):425-37. [DOI:10.18632/aging.100038] [PMID] [PMCID] [DOI:10.18632/aging.100038]
10. Gatica D, Chiong M, Lavandero S, Klionsky DJ. Molecular mechanisms of autophagy in the cardiovascular system. Circulation Research. 2015; 116(3):456-67. [DOI:10.1161/CIRCRESAHA.114.303788] [PMID] [PMCID] [DOI:10.1161/CIRCRESAHA.114.303788]
11. Lu J, Pan SS, Wang QT, Yuan Y. Alterations of cardiac KATP channels and autophagy contribute in the late cardioprotective phase of exercise preconditioning. International Heart Journal. 2018; 59(5):1106-15. [DOI:10.1536/ihj.17-003] [PMID] [DOI:10.1536/ihj.17-003]
12. Yan Z, Lira VA, Greene NP. Exercise training-induced regulation of mitochondrial quality. Exercise and Sport Sciences Reviews. 2012; 40(3):159-64. [DOI:10.1097/JES.0b013e3182575599] [DOI:10.1097/JES.0b013e3182575599]
13. Zhang L, Niu W, He Z, Zhang Q, Wu Y, Jiang C, et al. Autophagy suppression by exercise pretreatment and p38 inhibition is neuroprotective in cerebral ischemia. Brain Research. 2014; 1587:127-32. [DOI:10.1016/j.brainres.2014.08.067] [PMID] [DOI:10.1016/j.brainres.2014.08.067]
14. Garekani ET, Mohebbi H, Kraemer RR, Fathi R. Exercise training intensity/ volume affects plasma and tissue adiponectin concentrations in the male rat. Peptides. 2011; 32(5):1008-12. [DOI:10.1016/j.peptides.2011.01.027] [PMID] [DOI:10.1016/j.peptides.2011.01.027]
15. Ranjbar K, Zarrinkalam E, Salehi I, Komaki A, Fayazi B. Cardioprotective effect of resistance training and Crataegus oxyacantha extract on ischemia reperfusion–induced oxidative stress in diabetic rats. Biomedicine & Pharmacotherapy. 2018; 100:455-60. [DOI:10.1016/j.biopha.2018.02.021] [PMID] [DOI:10.1016/j.biopha.2018.02.021]
16. Pfaffl MW. A new mathematical model for relative quantification in real-time RT–PCR. Nucleic Acids Research. 2001; 29(9):e45. [PMID] [PMCID] [DOI:10.1093/nar/29.9.e45] [PMID] [PMCID]
17. Brown DA, Jew KN, Sparagna GC, Musch TI, Moore RL. Exercise training preserves coronary flow and reduces infarct size after Ischemia-Reperfusion in rat heart. Journal of Applied Physiology. 2003; 95(6):2510-8. [DOI:10.1152/japplphysiol.00487.2003] [PMID] [DOI:10.1152/japplphysiol.00487.2003]
18. Lee Y, Min K, Talbert EE, Kavazis AN, Smuder AJ, Willis WT, et al. Exercise protects cardiac mitochondria against Ischemia-Reperfusion injury. Medicine and Science in Sports and Exercise. 2012; 44(3):397-405. [DOI:10.1249/MSS.0b013e318231c037] [PMID] [DOI:10.1249/MSS.0b013e318231c037]
19. Rahimi M, Shekarforoush S, Asgari AR, Khoshbaten A, Rajabi H, Bazgir B, et al. The effect of high intensity interval training on cardioprotection against Ischemia-Reperfusion injury in wistar rats. EXCLI Journal. 2015; 14:237-46. [DOI;10.17179/excli2014-587] [PMID] [PMCID] [PMID] [PMCID]
20. Wang JY, Xia Q, Chu KT, Pan J, Sun LN, Zeng B, et al. Severe global cerebral ischemia-induced programmed necrosis of hippocampal CA1 neurons in rat is prevented by 3-methyladenine: A widely used inhibitor of autophagy. Journal of Neuropathology & Experimental Neurology. 2011; 70(4):314-22. [DOI:10.1097/NEN.0b013e31821352bd] [PMID] [DOI:10.1097/NEN.0b013e31821352bd]
21. Wen YD, Sheng R, Zhang LS, Han R, Zhang X, Zhang XD, et al. Neuronal injury in rat model of permanent focal cerebral ischemia is associated with activation of autophagic and lysosomal pathways. Autophagy. 2008; 4(6):762-9. [DOI:10.4161/auto.6412] [PMID] [DOI:10.4161/auto.6412]
22. Smuder AJ, Kavazis AN, Min K, Powers SK. Doxorubicin-induced markers of myocardial autophagic signaling in sedentary and exercise trained animals. Journal of Applied Physiology. 2013; 115(2):176-85. [DOI:10.1152/japplphysiol.00924.2012] [PMID] [DOI:10.1152/japplphysiol.00924.2012]
| بازنشر اطلاعات | |
 |
این مقاله تحت شرایط Creative Commons Attribution-NonCommercial 4.0 International License قابل بازنشر است. |
