نوع مقاله : مقاله پژوهشی
نویسندگان
1 دکترای فیزیولوژی ورزش، دانشگاه آزاد اسلامی، واحد تهران مرکز، تهران، ایران.
2 استاد، گروه فیزیولوژی ورزش، دانشگاه آزاد اسلامی، واحد تهران مرکز، تهران، ایران.
چکیده
زمینه و هدف: استرس زودرس به عنوان عامل خطر توسعه افسردگی و آسیبهای مرتبط با آن شناخته شدهاست. کاردیومیوپاتی نقش مهمی در پاتوفیزیولوژی افسردگی و بیماریهای قلبی - عروقی بازی میکند. شواهد نشان میدهد که فعالیت بدنی منظم در دوران نوجوانی ممکن است بتواند اثرات منفی استرس جدایی از مادر را به عنوان یک مدل حیوانی معتبر افسردگی بر رفتار و عملکرد میتوکندریایی قلبی رتهای بالغ تعدیل کند. روش تحقیق: در این مطالعۀ تجربی، استرس جدایی از مادر در 72 نوزاد رت صحرایی نر بوسیلۀ جدایی آن ها از مادرانشان برای 180 دقیقه در روز پس از زایمان روز دوم تا چهاردهم اعمال شد. سپس حیوانات به طور تصادفی در گروههای مختلف دوازده تایی (فلوکستین و نوارگردان) تقسیم شدند و معالجات را طی دوران بلوغ دریافت نمودند. سرانجام اثرات استرس جدایی از مادر در آزمونهای رفتاری رتها ارزیابی شد. نهایتاً، گونههای اکسیژن واکنشی، گلوتاتیون میتوکندریایی، ATP و رهایش سیتوکروم c در بافت قلبی حیوانات اندازه گیری گردید. با استفاده از آزمون t مستقل و تحلیل واریانس یک طرفه و در سطح معنی داری 05/0≥p؛ داده ها تجزیه و تحلیل شدند. یافتهها: رفتارهای شبه افسردگی بدنبال استرس جدایی از مادر در رتهای صحرایی نر بالغ با اختلال عملکرد میتوکندری قلبی در حیوانات همراه بود. علاوه بر این، نتایج نشان داد که درمان حیوانات با فلوکستین و تمرین اجباری روی نوارگردان طی دوره نوجوانی برخی رفتارهای حیوانی و عملکردهای میتوکندری قلبی را بهبود میبخشد. نتیجهگیری: نتایج این مطالعه قویاً بیانگر اهمیت نوجوانی به عنوان دورهای است که طی آن درمان حیوانات با اجرای تمرین نوارگردان، اثرات محافظتی قابل توجهی بر اختلالات هموستاز انرژی قلبی ناشی از استرس جدایی از مادر دارد.
کلیدواژه‌ها
عنوان مقاله [English]
Effects of mandatory aerobic exercise in adolescence on the negative impact of maternal separation stress on cardiac oxidative stress in adult male rat
نویسندگان [English]
- Ehtram alsadat Sahafi 1
- Maghsoud Peeri 2
1 PhD of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
2 Full Professor, Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
چکیده [English]
Background and Aim: Early life stress is known as a risk factor for the development of depression and its associated comorbidities. Mitochondrial dysfunction plays a critical role in the pathophysiology of depression and cardiovascular diseases. Evidence indicated that regular physical activity during adolescence may be able to adjust the negative impact of maternal separation stress as a valid animal model of depression on behavior and cardiac mitochondrial function of adult rats. Materials and Methods: In this experimental study, maternal separation stress was applied to 72 male rat pups by separating them from their mothers for 180 minutes during second to fourteenth day of postnatal. Then, the animals were randomly divided into different treatment six groups (fluoxetine and treadmill) and received the treatments during adolescence. Further, we evaluated the effects of maternal separation stress on the rat behaviors test. Finally, we assessed the reactive oxygen species, mitochondrial glutathione, ATP and cytochrome c release in the cardiac tissue of animals. Comparison between groups were analyzed using independent t-test and one-way analysis of variance and statistically significant was considered if p≤0.05. Result: The results of this study showed tha depressive-like behaviors following maternal separation stress in adult male rats were associated with oxidative stress in cardiac tissue. Also the results showed that treating animals with fluoxetine or compulsory exercise on the treadmill during adolescence improved some cardiac mitochondrial function. Conclusion: The results of this study highlights the importance of adolescence as a period during which treating animals by performing a treadmill exercise has significant protective effects on cardiac energy homeostasis disorders caused by maternal separation stress.
کلیدواژه‌ها [English]
- Maternal separation stress
- Cardiomiopaty
- Mandatory aerobic exercise
- Reactive oxygen species
Amiri, S., Amini-Khoei, H., Mohammadi-Asl, A., Alijanpour, S., Haj-Mirzaian, A., Rahimi-Balaei, M., ... & Zarrindast, M. R. (2016). Involvement of D1 and D2 dopamine receptors in the antidepressant-like effects of selegiline in maternal separation model of mouse. Physiology & Behavior, 163, 107-114.
Ballinger, S. W. (2005). Mitochondrial dysfunction in cardiovascular disease. Free Radical Biology and Medicine, 38 (10), 1278-1295.
Cryan, J. F., Markou, A., & Lucki, I. (2002). Assessing antidepressant activity in rodents: Recent developments and future needs. Trends in Pharmacological Sciences, 23(5), 238-245.
Daniels, W. M., Marais, L., Stein, D. J., & Russell, V. A. (2012). Exercise normalizes altered expression of proteins in the ventral hippocampus of rats subjected to maternal separation. Experimental Physiology, 97(2), 239-247.
Gao, P., Qian, D. H., Li, W., & Huang, L. (2009). Npra-mediated suppression of angii-induced ros production contribute to the antiproliferative effects of b-type natriuretic peptide in vsmc. Molecular and Cellular Biochemistry, 324(1-2), 165.
Gawryluk, J. W., Wang, J. F., Andreazza, A. C., Shao, L., & Young, L. T. (2011). Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders. International Journal of Neuropsychopharmacology, 14(1), 123-130.
Glassman, A. H. (2007). Depression and cardiovascular comorbidity. Dialogues in Clinical Neuroscience, 9(1), 9.
Green, D. R., & Kroemer, G. (2004). The pathophysiology of mitochondrial cell death. Science, 305(5684), 626-629.
Grippo, A. J. (2009). Mechanisms underlying altered mood and cardiovascular dysfunction: The value of neurobiological and behavioral research with animal models. Neuroscience & Biobehavioral Reviews, 33(2), 171-180.
Haj-Mirzaian, A., Amiri, S., Kordjazy, N., Momeny, M., Razmi, A., Rahimi-Balaei, M., ... & Dehpour, A. R. (2016). Lithium attenuated the depressant and anxiogenic effect of juvenile social stress through mitigating the negative impact of interlukin-1β and nitric oxide on hypothalamic–pituitary–adrenal axis function. Neuroscience, 315, 271-285.
Hosseini, M. J., Shaki, F., Ghazi-Khansari, M., & Pourahmad, J. (2014). Toxicity of copper on isolated liver mitochondria: impairment at complexes I, II, and IV leads to increased ROS production. Cell Biochemistry and Biophysics, 70(1), 367-381.
Janssen, I., & LeBlanc, A. G. (2010). Systematic review of the health benefits of physical activity and fitness in school-aged children and youth. International Journal of Behavioral Nutrition and Physical Activity, 7(1), 40.
Klinedinst, N. J., & Regenold, W. T. (2015). A mitochondrial bioenergetic basis of depression. Journal of Bioenergetics and Biomembranes, 47(1-2), 155-171.
Leasure, J., & Jones, M. (2008). Forced and voluntary exercise differentially effect brain and behavior. Neuroscience, 156(3), 456-465.
Lesnefsky, E. J., Moghaddas, S., Tandler, B., Kerner, J., & Hoppel, C. L. (2001). Mitochondrial dysfunction in cardiac disease: Ischemia–reperfusion, aging, and heart failure. Journal of Molecular and Cellular Cardiology, 33(6), 1065-1089.
Li, P., Nijhawan, D., Budihardjo, I., Srinivasula, S. M., Ahmad, M., Alnemri, E. S., & Wang, X. (1997). Cytochrome c and datp-dependent formation of apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell, 91(4), 479-489.
Lichtman, J. H., Bigger Jr, J. T., Blumenthal, J. A., Frasure-Smith, N., Kaufmann, P. G., Lespérance, F., ... & Froelicher, E. S. (2008). Depression and coronary heart disease: recommendations for screening, referral, and treatment: a science advisory from the American heart association prevention committee of the council on cardiovascular Nursing, council on clinical cardiology, council on epidemiology and prevention, and Interdisciplinary council on quality of care and outcomes research: endorsed by the American Psychiatric Association. Circulation, 118(17), 1768-1775.
Liesa, M., & Shirihai, O. S. (2013). Mitochondrial dynamics in the regulation of nutrient utilization and energy expenditure. Cell Metabolism, 17(4), 491-506.
Maes, M., Ruckoanich, P., Chang, Y. S., Mahanonda, N., & Berk, M. (2011). Multiple aberrations in shared inflammatory and oxidative & nitrosative stress (IO&NS) pathways explain the co-association of depression and cardiovascular disorder (CVD), and the increased risk for CVD and due mortality in depressed patients. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 35(3), 769-783.
O'keefe, J. H., Patil, H. R., Lavie, C. J., Magalski, A., Vogel, R. A., & McCullough, P. A. (2012). Potential adverse cardiovascular effects from excessive endurance exercise. Paper presented at the Mayo Clinic Proceedings, 87 (6), 587-595.
Peeri, M., & Amiri, S. (2015). Protective effects of exercise in metabolic disorders are mediated by inhibition of mitochondrial-derived sterile inflammation. Medical Hypotheses, 85(6), 707-709.
Powers, S., Sollanek, K., Wiggs, M., Demirel, H., & Smuder, A. (2014). Exercise-induced improvements in myocardial antioxidant capacity: The antioxidant players and cardioprotection. Free Radical Research, 48(1), 43-51.
Saadati, H., Esmaeili-Mahani, S., Esmaeilpour, K., Nazeri, M., Mazhari, S., & Sheibani, V. (2015). Exercise improves learning and memory impairments in sleep deprived female rats. Physiology & Behavior, 138, 285-291.
Sadeghi, M., Peeri, M., & Hosseini, M. J. (2016). Adolescent voluntary exercise attenuated hippocampal innate immunity responses and depressive-like behaviors following maternal separation stress in male rats. Physiology & Behavior, 163, 177-183.
Sahafi, E., Peeri, M., Hosseini, M. J., & Azarbyjani, M. A. (2018). Cardiac oxidative stress following maternal separation stress was mitigated following adolescent voluntary exercise in adult male rat. Physiology & Behavior, 183, 39-45.
Shaki, F., Hosseini, M. J., Ghazi-Khansari, M., & Pourahmad, J. (2012). Toxicity of depleted uranium on isolated rat kidney mitochondria. Biochimica et Biophysica Acta (BBA)-General Subjects, 1820(12), 1940-1950.
Sonei, N., Amiri, S., Jafarian, I., Anoush, M., Rahimi-Balaei, M., Bergen, H., ... & Hosseini, M. J. (2017). Mitochondrial dysfunction bridges negative affective disorders and cardiomyopathy in socially isolated rats: pros and cons of fluoxetine. The World Journal of Biological Psychiatry, 18(1), 39-53.
Steptoe, A., & Kivimäki, M. (2013). Stress and cardiovascular disease: An update on current knowledge. Annual Review of Public Health, 34, 337-354.
Suematsu, N., Tsutsui, H., Wen, J., Kang, D., Ikeuchi, M., Ide, T., ... & Takeshita, A. (2003). Oxidative stress mediates tumor necrosis factor-α induced mitochondrial DNA damage and dysfunction in cardiac myocytes. Circulation, 107 (10), 1418-1423.
Sun, L. N., Li, X. L., Wang, F., Zhang, J., Wang, D. D., Yuan, L., ... & Qi, J. S. (2017). High‐intensity treadmill running impairs cognitive behavior and hippocampal synaptic plasticity of rats via activation of inflammatory response. Journal of Neuroscience Research, 95(8), 1611-1620.
Taylor, R. S., Sagar, V. A., Davies, E. J., Briscoe, S., Coats, A. J., Dalal, H., ... & Singh, S. (2019). Exercise-based rehabilitation for heart failure: cochrane systematic review, meta-analysis, and trial sequential analysis. JACC: Heart Failure, 7(8), 691-705.
Trivedi, M. H., Rush, A. J., Wisniewski, S. R., Nierenberg, A. A., Warden, D., Ritz, L., ... & Shores-Wilson, K. (2006). Evaluation of outcomes with citalopram for depression using measurement-based care in STAR* D: implications for clinical practice. American Journal of Psychiatry, 163(1), 28-40.
Turdi, S., Yuan, M., Leedy, G. M., Wu, Z., & Ren, J. (2012). Chronic social stress induces cardiomyocyte contractile dysfunction and intracellular ca2+ derangement in rats. Physiology & Behavior, 105(2), 498-509.
)