اثر تمرین هوازی و مکمل‌دهی مایتوکیو (MitoQ) بر بیان ژن‌های OPA1 و FIS1 درگیر در مسیر دینامیک میتوکندریایی بافت میوکارد رت‌های نر پیر

نوع مقاله : مقاله پژوهشی

نویسندگان

1 دانشجوی دکتری فیزیولوژی ورزش، گروه فیزیولوژی ورزشی، واحد تهران مرکزی، دانشگاه آزاد اسلامی، تهران، ایران

2 استادیار گروه تربیت بدنی و علوم ورزشی، واحد دزفول، دانشگاه آزاد اسلامی، دزفول، ایران

3 استادیار گروه تربیت بدنی و علوم ورزشی، واحد خدابنده، دانشگاه آزاد اسلامی، خدابنده، ایران.

چکیده

زمینه و هدف: یکی از مشکلات در بیشتر کشورهای جهان، مسئله پیری جمعیت و پیامدهای ناشی از آن در بروز بیماری‌های قلبی است. هدف از مطالعه حاضر، بررسی تاثیر تمرین هوازی و مکمل‌دهی مایتوکیو بر عوامل درگیر در مسیر سیگنالینگ دینامیک میتوکندریایی شامل اپتیک آتروفی-۱ (OPA1) و پروتئین فیژن میتوکندریایی-1 (FIS1) در بافت قلب موش‌های پیر نر است. روش تحقیق: در مطالعه تجربی حاضر، تعداد ۲۸ سر موش صحرایی نر پیر نژاد ویستار به‌‌صورت تصادفی در چهار گروه هفت‌تایی شامل کنترل، تمرین هوازی، مکمل مایتوکیو، و تمرین هوازی+‌مکمل مایتوکیو تقسیم شدند. حیوانات پس از آشناسازی با محیط به مدت هشت هفته (پنج روز در هفته) تمرین هوازی با شدت ۷۰ درصد سرعت بیشینه را انجام دادند. مکمل‌دهی مایتوکیو به مدت هشت هفته به صورت محلول در آب خوراکی با غلظت ۲۵۰ میکرومولار انجام شد. برای ارزیابی متغیرها در بافت قلب از روش Real-time PCR استفاده گردید. آنالیز آماری داده‌ها با استفاده از آزمون تحلیل واریانس دو راهه و آزمون تعقیبی توکی در سطح معنی‌‌داری ۰۵/۰>p انجام گردید. یافته ها: تمرین هوازی به‌‌‌طور معنی‌‌داری بیان ژن FIS1 را در بافت میوکارد کاهش (۰۰۶/۰=p) و مکمل مایتوکیو میزان بیان ژن OPA1 را در بافت قلب موش‌های پیر افزایش داد (۰۴/p=0)؛ اما بر بیان ژن FIS1 تاثیر معنی‌‌داری نداشت (۰۶/p=0). از طرفی، ترکیب مایتوکیو و تمرین، بیان ژن دو متغیر FIS1 و OPA1 را نسبت به مکمل مایتوکیو، به‌‌طور معنی‌‌داری کاهش داد (۰۲/p=0). نتیجه گیری: مکمل مایتوکیو در نقش یک آنتی‌‌اکسیدان پیشرفته احتمالاً می‌تواند در دینامیک میتوکندریایی عضله قلبی پیر نقش داشته باشد و بیان ژن فرآیند همجوشی را بهبود ‌‌بخشد. با این حال، ترکیب تمرین هوازی و مایتوکیو می‌‌تواند فرآیند همجوشی و شکافت میتوکندریایی را تعدیل کند.

کلیدواژه‌ها

عنوان مقاله [English]

The effect of aerobic training and MitoQ supplementation on the gene expression of OPA1 and FIS1 in myocardial mitochondrial dynamic pathway in old male rats

نویسندگان [English]

  • Sadollah Salarmohammadi 1
  • Elham Farhadfar 2
  • Zahra Sarlak 3
1 PhD. Student at Department of Sport Physiology, CT. C., Islamic Azad University, Tehran, Iran
2 Assistant professor at Department of Physical Education and sport Science, Dez. C., Islamic Azad University, Dezful, Iran.
3 Assistant professor at Department of Physical Education and Sport Sciences, Khod.C., Islamic Azad University, Khodabandeh, Iran.
چکیده [English]

Extended abstract
Background and Aim: Aging is a complex biological process characterized by progressive functional decline, ultimately reducing quality of life. Cardiovascular diseases and their related mortality are markedly more prevalent in older adults, with aging recognized as a major risk factor for cardiovascular dysfunction. Mitochondrial impairment has been identified as a critical contributor to age-related cardiac deterioration. Proteins regulating mitochondrial dynamics, such as optic atrophy-1 (OPA1) and mitochondrial fission protein-1 (FIS1), play a key role in maintaining mitochondrial integrity and cellular homeostasis. Aerobic exercise training and MitoQ—an antioxidant targeting mitochondrial oxidative stress—have both been proposed as non-pharmacological interventions capable of improving mitochondrial function in aging. Therefore, the present study aimed to investigate the effects of aerobic exercise training and MitoQ supplementation on OPA1 and FIS1 expression in the cardiac tissue of aged male rats.
Materials and methods: In this experimental study, 28 aged male Wistar rats were obtained from the Kerman physiology research center. After a one-week acclimation period under controlled laboratory conditions, animals were randomly assigned into four groups (n=7 per group): control, aerobic exercise, MitoQ supplementation, and combined aerobic exercise+MitoQ supplementation.
To determine training intensity, maximal oxygen consumption (VO₂max) was estimated based on maximal running speed (Vmax). Aerobic exercise training was performed for eight weeks, with session intensity adjusted according to the established relationship between treadmill speed and calculated VO₂max. Rats in the control and MitoQ groups did not perform training but were placed on the treadmill without running during the training sessions to equalize environmental stress exposure. MitoQ was administered only to the designated MitoQ (250µm) and combined intervention groups.
At the end of the intervention period, cardiac tissue samples were collected, and gene expression levels of OPA1 and FIS1 were quantified using the 2^-ΔΔCt method, with 18S rRNA serving as the internal reference gene. The data was analyzed statistically using a two-way ANOVA test.
Results: Expression of the FIS1 gene was up-regulated in the cardiac tissue of aged male rats. Post-hoc analysis revealed that aerobic exercise significantly reduced FIS1 expression compared to the control group (p=0.006). In addition, the combined intervention of aerobic exercise and MitoQ supplementation significantly decreased the expression of both FIS1 and OPA1 compared to the MitoQ-only group (p=0.02). MitoQ supplementation alone significantly increased OPA1 gene expression in the cardiac tissue compared to the control group (p=0.04). A significant reduction in body weight was observed beginning in week 6 in both the aerobic exercise group and the combined aerobic exercise+MitoQ group (p=0.001).
Conclusion: The findings of this study indicate that the antioxidant MitoQ supplementation influences mitochondrial fission and thereby alters mitochondrial dynamics in the cardiac tissue of aged rats. Furthermore, when combined with aerobic exercise, a modulatory effect on these mitochondrial processes was observed. This interaction may be attributed to exercise-induced oxidative stress, through which exercise appears to modify the impact of MitoQ on mitochondrial fission and fusion mechanisms in the heart. Collectively, these results highlight the potential of integrating antioxidant therapy with aerobic training to regulate age-associated mitochondrial alterations in cardiac tissue.
Ethical considerations: The present project has a code of ethics for working with laboratory animals, number IR-KHU.KRC.1000.250, from the Ethics Committee of the Institute of Movement Sciences, Kharazmi University, IRAN.
Compliance with ethical guidelines: In the present project, all work with laboratory animals was carried out according to the ethical charter, and the necessary standards were observed in the project.
Funding: This article is an excerpt from a doctoral dissertation by a student at Islamic Azad University, Central Tehran Branch.
Conflict of interest: There is no conflict of interest between authors.
 

کلیدواژه‌ها [English]

  • Aerobic exercise
  • MitoQ supplement
  • Myocardial tissue
  • Mitochondrial biogenesis

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مطالعات کاربردی علوم زیستی در ورزش
دوره 13، شماره 36
دی 1404
صفحه 58-71

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