نوع مقاله : مقاله پژوهشی Released under CC BY-NC 4.0 license I Open Access I

نویسندگان

1 دانشجوی دکتری ،گروه تربیت بدنی و علوم ورزشی، دانشکدۀ علوم انسانی، دانشگاه تربیت مدرس، تهران، ایران

2 دانشیار، گروه تربیت بدنی و علوم ورزشی، داﻧﺸﻜﺪة ﻋﻠﻮم اﻧﺴﺎﻧﻲ، داﻧﺸﮕﺎه ﺗﺮﺑﻴﺖ ﻣﺪرس، تهران، ایران

3 . استادیار، گروه تربیت بدنی و علوم ورزشی، دانشکدۀ ادبیات و علوم انسانی، دانشگاه لرستان، خرم‌آباد، ایران

4 استاد، گروه علوم تشریح، دانشکدۀ علوم پزشکی، دانشگاه تربیت مدرس، تهران، ایران

چکیده

گلیکوژن سنتازکیناز3 بتا، کلید تنظیمی است که خروجی بسیاری از مسیرهای پیام­رسانی را تعیین می­کند. مهار آن در افزایش بقای نورونی مؤثر گزارش شده ­است. ازاین­رو پژوهش حاضر به بررسی اثر شش هفته تمرین استقامتی بر بیان ژن GSK-3β در بخش حرکتی نخاع رت­های نر ویستار با نوروپاتی دیابت می­پردازد. بدین منظور 16 سر رت نر ویستار به­طور تصادفی به چهار گروه سالم کنترل، سالم تمرین، نوروپاتی کنترل و نوروپاتی تمرین تقسیم شدند. برای القای دیابت از روش تزریق درون‌صفاقی محلول استرپتوزوسین (45 میلی­گرم/کیلوگرم) استفاده شد. دو هفته پس از تزریق استرپتوزوسین، با اثبات نوروپاتی دیابت توسط آزمون­های آلودینای ­مکانیکی و هایپرآلژزیای ­حرارتی، برنامۀ تمرین استقامتی با شدت متوسط به مدت شش هفته اجرا شد. 24 ساعت پس از آخرین جلسۀ تمرینی، رت‌ها تشریح و نورون‌های حرکتی L4-L6 بافت نخاع استخراج شد. بررسی بیان ژن نیز با روش Real Time-PCR صورت گرفت. تجزیه‌وتحلیل آماری نشان داد در مقایسه با گروه نوروپاتی کنترل، نوروپاتی تمرین کاهش بیان GSK-3β را تجربه می­کند (02/0= P) ؛ از سوی دیگر اختلاف معناداری بین گروه­های سالم کنترل و نوروپاتی کنترل دیده شد
(02/0= P)، به­طوری­که بیان ژن در گروه نوروپاتی کنترل افزایش نشان داد، اما اختلاف گروه کنترل سالم و نوروپاتی تمرینی معنادار نبود. براساس نتایج این تحقیق یکی از عوامل احتمالی درگیر در گسترش آسیب نورون‌های حرکتی نوروپاتی دیابت، تنظیم افزایشی mRNAGSK-3β است و ورزش به‌عنوان یک راهبرد غیردارویی، می‌تواند آن را تعدیل و به سطوح نرمال نزدیک کند. بنابراین، پیشنهاد می‌شود GSK-3β به‌عنوان یک هدف درمانی بدیع در بیماری دیابت مورد توجه قرار گیرد.

کلیدواژه‌ها

عنوان مقاله [English]

The Effect of 6 Weeks of Endurance Training on Gene Expression of GSK-3β in the Motor Area of the Spinal Cord of Male Wistar Rats with Diabetic Neuropathy

نویسندگان [English]

  • Faranak Sadeghi 1
  • Reza GHarakhanlou 2
  • Masoud Rahmati 3
  • Mansoureh Movahedin 4

1 .PhD Student, Department of Physical Education and Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran

2 Assosiate Professor, Department of Physical Education and Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran

3 Assistant Professor, Department of Physical Education and Sport Sciences, Faculty of Literature and Humanities, Lorestan University, Khoram Abaad, Iran

4 Professor, Department of Anatomical Sciences, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran

چکیده [English]

Glycogen synthase kinase 3 beta is a regulator key of many signaling pathways. It is reported that inhibition of this kinase increases neuronal survival. Accordingly, in this study, the effect of 6 weeks of endurance training on the gene expression of GSK-3β in the motor area of the spinal cord of male Wistar rats with diabetic neuropathy was investigated. For this aim, 16 male Wistar rats were randomly assigned to four groups: healthy control, healthy trained, neuropathy control, neuropathy trained. Intraperitoneal injection of a STZ (streptozotocin) solution (45 mg/kg) was used to induce diabetes. 2 weeks after STZ injection, the mechanical allodynia and thermal hyperalgesia tests demonstrated the diabetic neuropathy. A moderate endurance training protocol was performed for 6 weeks. 24 hours after the last training session, the rats were sacrificed and the L4-L6 motor neurons of the spinal cord tissue were removed. GSK-3β mRNA expression was performed using Real Time-PCR. Statistical analysis showed that neuropathy trained group experienced a decrease in the GSK-3β expression compared with neuropathy control group (P=0.02). On the other hand, there was a significant difference between healthy control and neuropathy control groups (P=0.02), that is to say the gene expression increased in neuropathy control group. However, there was no significant difference between healthy control and neuropathy trained groups. The results show that one of the factors involved in the spread of damage to motor neurons of diabetic neuropathy is incremental regulation of mRNAGSK-3β and training as a non-pharmacotherapy strategy can modulate and return it to normal levels. Therefore, it is suggested that GSK-3β should receive attention as a novel treatment target in diabetes.

کلیدواژه‌ها [English]

  • diabetic neuropathy
  • Endurance training
  • GSK-3β
  • motor area of spinal cord
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