مقایسه تاثیر دو نوع تمرین هوازی بر روی بیان ژن GDNF و گیرنده آن GFRα1 در رت های دچار ضایعه نخاعی

نوع مقاله : مقاله پژوهشی

نویسندگان

1 دانشجوی دکتری،گروه تربیت بدنی و علوم ورزشی، واحد بجنورد،دانشگاه آزاد اسلامی، بجنورد، ایران.

2 استادیار گروه علوم ورزشی، دانشگاه آزاد اسلامی، واحد بجنورد، بجنورد، ایران(نویسنده مسئول)

3 استادیار گروه فیزیک پزشکی و رادیولوژی، دانشگاه علوم پزشکی خراسان شمالی، بجنورد، ایران

4 استادیار، گروه تربیت بدنی و علوم ورزشی، واحد بجنورد،دانشگاه آزاد اسلامی، بجنورد، ایران.

چکیده

مقدمه: هدف از این مطالعه بررسی چهار هفته تمرین هوازی منتخب بر بیان ژن GDNF و گیرنده آن GFRα1 در هیپوکامپ رت های مبتلا به ضایعه نخاعی بود.
روش کار: در این مطالعه تجربی، رت ها به صورت تصادفی به 6 گروه تقسیم شدند. حیوانات تحت بیهوشی عمومی و از طریق جراحی ستون فقرات T11-T9  مورد ضایعه نخاعی قرار گرفتند و پس از گذشت دو هفته ریکاوری تمرینات هوازی در دو مدل بر روی آن ها اجرا شد. پس از تمرین بافت هیپوکامپ مغزی جهت بررسی بیان ژن فاکتور GDNF و گیرنده آن GFRα1 برداشته شد.
نتایج:  بیان ژنGDNF  در مدل آسیب نخاعی نسبت به گروه کنترل کاهش معناداری داشت، همچنین بیان این ژن در گروه آسیب نخاعی تمرین اول و در گروه آسیب نخاعی تمرین دوم نسبت به گروه آسیب نخاعی افزایش داشت؛ اما این افزایش بین دو گروه آسیب نخاعی با دو تمرین هوازی تفاوت معناداری را نشان نداد. بیان ژن گیرنده GFRα1  در مدل آسیب نخاعی نسبت به گروه کنترل کاهش معناداری داشت. بیان این ژن در گروه آسیب نخاعی تمرین اول و در گروه آسیب نخاعی تمرین دوم نسبت به گروه آسیب نخاعی افزایش داشت؛ اما این افزایش بین دو گروه آسیب نخاعی با دو تمرین هوازی تفاوت معناداری را نشان نداد. نتیجه‌گیری: پروتکل های تمرینی این مطالعه باعث افزایش بیان ژن GDNF و گیرنده آن GFRα1  در رت های ضایعه نخاعی شده و میتوان آن را به عنوان عامل کمک کننده به رشد عصبی و و بقای نرونی در مدل های ضایعه نخاعی در نظر گرفت.

کلیدواژه‌ها

موضوعات


عنوان مقاله [English]

Comparison of the effect of two types of aerobic exercise on the expression of GDNF gene and its receptor GFRα1 in Spinally Injured Rats

نویسندگان [English]

  • Sina Jalili Rasti 1
  • Sadegh Cheragh Birjandi 2
  • Mohammad YounesiHeravi 3
  • Ali Yaghoubi 4
1 Ph.D Candidate, Department of Physical Education and Sport Sciences, Bojnourd Branch, Islamic Azad University, Bojnourd, Iran.
2 Assistant Professor, Department of Sport Science, Islamic Azad University, Bojnurd Branch, Bojnurd, Iran
3 Assistant Professor, Department of medical physics and radiology, North Khorasan University of Medical Sciences, Bojnurd, Iran.
4 Assistant Professor, Department of Physical Education and Sport Sciences, Bojnourd Branch, Islamic Azad University, Bojnourd, Iran.
چکیده [English]

Introduction
This study aimed to investigate 4-weeks of selected aerobic training on the expression of GDNF gene and its receptor GFRα1 in hippocampal rats with spinal cord injury (SCI).
Material and Method
In this experimental study, rats were randomly divided into 6 groups. Animals were subjected to spinal cord injury under general anesthesia and T11-T9 spine surgery, and after 2 weeks of recovery, aerobic exercises were performed on them. After training, hippocampal tissue was removed to examine the gene expression.
Results
The expression of GDNF in the SCI model was significantly decreased compared to the control group, and the expression of this gene was increased in the SCI group of the first exercise and in the SCI group of the second exercise compared to the SCI group; However, this increase did not show a significant difference between the two SCI groups. The expression of the GFRα1 receptor in the SCI model had a significant decrease compared to the control group. This expression was increased in the SCI group of the first exercise and in the SCI group of the second exercise compared to the SCI group; However, this increase did not show a significant difference between the two SCI groups.
Conclusion
The training protocols of this study increased the expression of the GDNF gene and its receptor GFRα1 in SCI rats, and it can be considered as a contributing factor to neural growth and neuronal survival in SCI models.

کلیدواژه‌ها [English]

  • Aerobic Exercise
  • Spinal Cord Injury
  • GDNF
  • GFRα1
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