اثر تمرین هوازی و پیش شرطی سازی ایسکمی دور بر بیان ژن بکلین-1 بافت قلب موشهای بزرگ آزمایشگاهی دیابتی

نوع مقاله : مقاله پژوهشی

نویسندگان

1 گروه فیزیولوژی ورزشی، دانشکده انسانی، واحد ساری، دانشگاه آزاد اسلامی، ساری، ایران

2 گروه قلب، مرکز تحقیقات قلب و عروق، دانشگاه علوم پزشکی مازندران، ساری، ایران

چکیده

مقدمه و هدف: با وجود اثر محافظتی پیش شرطی­سازی ایسکمی از بافتها، اثر آن بر اتوفاژی افزایش­یافته ناشی از دیابت به روشنی مشخص نیست. اتوفاژی می­تواند با فعالیت ورزشی مهار یا فعال شود. هدف از مطالعه‌ی حاضر، بررسی اثر تمرین استقامتی و پیش شرطی­سازی ایسکمی دور بر بیان ژن بکلین-1 بافت قلب موش‌ها دیابتی بود.
مواد و روش ها: در این مطالعه تجربی، 35 موش ویستار به‌صورت تصادفی به 7 گروه: کنترل سالم، دیابتی، دیابتی ایسکمی یک پا، دیابتی ایسکمی دو پا، دیابتی تمرین استقامتی، دیابتی تمرین+ایسکمی یک پا، دیابتی تمرین+ایسکمی دو پا تقسیم شدند. پیش شرطی­سازی ایسکمی شامل سه دور 5 دقیقه­ای ایسکمی و 5 دقیقه رپرفیوژن متعاقب بود. تمرین استقامتی به مدت 6 هفته و 5 روز در هفته انجام شد و شامل دویدن روی تردمیل با سرعت 9 متر در دقیقه و مدت 15 دقیقه در هفته اول بود که در هفته ششم به سرعت 18 متر در دقیقه و مدت 30 دقیقه رسید. بیان ژن بکلین-1 با روش real-time PCR اندازه‌گیری گردید. از روش آماری واریانس یکطرفه و آزمون تعقیبی توکی استفاده شد.
نتایج: بیان ژن بکلین-1 افزایش معناداری در گروه دیابتی نسبت به گروه سالم داشت (0001/0P=). در مقایسه با گروه دیابت، ایسکمی یک پا (0001/0P=)، ایسکمی دو پا (0001/0P=)، تمرین (0001/0P=)، تمرین+ایسکمی یک پا (0001/0P=) و تمرین+ایسکمی دو پا (0001/0P=) منجر به کاهش معنی­دار بیان بکلین-1 بافت قلب شد.
نتیجه‌گیری: به نظر می­رسد که اثر پیش شرطی­سازی ایسکمی در کاهش بکلین-1 مستقل از حجم عضلانی درگیر ایسکمی است. تمرین استقامتی به‌همراه پیش شرطی­سازی ایسکمی اثر بیشتری در کاهش بکلین-1 بافت قلب موشهای دیابتی نسبت به تمرین و ایسکمی تنها دارد.

کلیدواژه‌ها

عنوان مقاله [English]

The effect of endurance training and remote ischemic preconditioning on myocardial Beclin-1 gene expression in diabetic rats

نویسندگان [English]

  • Fazeleh Akbarnia 1
  • Amin Farzaneh Hesari 1
  • Abdollah Hashemvarzi 1
  • Aliasghar Farsavian 2
1 Department of Exercise Physiology, Sari Branch, Islamic Azad University, Sari, Iran
2 Department of Cardiology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
چکیده [English]

Background and Objective: Despite the protective effect of ischemic preconditioning (IPC) from tissues, its effect on diabetes-induced excessive autophagy is not clear. Autophagy could be inhibited or activated through exercise. The present study aimed to investigate the effect of endurance training and remote IPC on myocardial Beclin-1 gene expression in diabetic rats.
Materials and Method: In this experimental research, 35 Wistar rats were randomly divided into seven groups: normal control (C), diabetic (D), diabetic one leg ischemia (OI), diabetic two legs ischemia (TI), diabetic endurance training (E), diabetes one leg ischemia + endurance training (OIE), diabetes two legs ischemia+ endurance training (TIE). IPC was included three 5-minute cycles of ischemia, followed by five minutes of reperfusion. The endurance training groups performed exercise training for six weeks and five days a week and was included running on a treadmill. The speed for the first week is set at 9 meters per minute for 15 minutes. By the sixth week, the training speed was increased to 18 meters per minute for 30 minutes. Beclin-1 gene expression was measured by RT-PCR. Data were analyzed by one-way analysis of variance and Tukey post hoc tests.
Results: Beclin-1 gene expression significantly increased in D group compared to C group (p=0.0001). Becli-1 gene expression significantly decreased in OI (p=0.0001), TI (p=0.0001), E (p=0.0001), OIE (p=0.0001) and TIE (p=0.0001) compared to the D.
Conclusion: It seems that the effect of ischemia preconditioning in decreasing Beclin-1 is independent of the ischemia-affected muscle mass. Endurance training with IPC is more effective in decreasing Beclin-1 in diabetes than any of the exercise and IPC interventions alone.

کلیدواژه‌ها [English]

  • Exercise training
  • Ischemic preconditioning
  • Autophagy
  • Beclin-1

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