Rahmati Masoud, Gharakhanlou Reza, Movahedin Mansoureh, Mowla Seyed Javad, Khazani Ali, Fouladvand Maryam, Jahani Golbar Shiva
Department of Physical Education and Sport Sciences, Faculty of Literature and Humanities, Lorestan University, Khorramābād, Iran.
Department of Physical Education and Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran.
Arch Iran Med. 2015 Feb;18(2):94-101.
Previous research has demonstrated diabetic-induced axonal transport deficits. However, the mechanism of axonal transport impairment induced by diabetes is poorly understood. Kinesin motor proteins have been shown to transport various cargos along highly polarized neurons. In the present study, we investigated the effect of regular treadmill exercise on KIF5B and Sunday Driver (SYD) mRNA levels in sensory and motor parts of spinal cord and KIF5B content in sciatic nerves of streptozotocin (STZ)-induced diabetic rats.
Forty male Wistar rats were divided into four groups: (1) diabetic trained (DT: n = 10); (2) Non-trained diabetic (NTD: n = 10); (3) normal control (NC: n = 10), and (4) normal trained (NT: n = 10). Two weeks after STZ injection (45 mg/kg, i.p.), the rats were subjected to treadmill exercise for 5 days a week over 6 weeks. We determined mRNA levels and protein content by Real time- PCR and ELISA.
Exercise training decreased blood glucose levels in the DT rats. Diabetes increased the KIF5B and SYD mRNA in both sensory and motor parts and KIF5B content in sciatic nerves in the NTD. Moreover, exercise training modulated the KIF5B and SYD mRNA and KIF5B content to normal levels in the DT. Exercise training in NT rats increased KIF5B and SYD mRNA in sensory and motor parts and KIF5B content in sciatic nerves.
Our results suggest that diabetes seems to change spinal cord KIF5B and SYD mRNA and sciatic nerves KIF5B content and exercise training modifies it, which may be attributable to the training-induced decreased hyperglycemia.
先前的研究已经证明糖尿病会导致轴突运输缺陷。然而,糖尿病诱导轴突运输受损的机制尚不清楚。驱动蛋白运动蛋白已被证明可沿高度极化的神经元运输各种货物。在本研究中,我们调查了规律的跑步机运动对链脲佐菌素(STZ)诱导的糖尿病大鼠脊髓感觉和运动部分中驱动蛋白家族成员5B(KIF5B)和周日驱动蛋白(SYD)mRNA水平以及坐骨神经中KIF5B含量的影响。
40只雄性Wistar大鼠分为四组:(1)糖尿病训练组(DT:n = 10);(2)未训练糖尿病组(NTD:n = 10);(3)正常对照组(NC:n = 10),以及(4)正常训练组(NT:n = 10)。腹腔注射STZ(45 mg/kg)两周后,大鼠每周进行5天跑步机运动,持续6周。我们通过实时聚合酶链反应(Real time-PCR)和酶联免疫吸附测定(ELISA)来测定mRNA水平和蛋白质含量。
运动训练降低了DT组大鼠的血糖水平。糖尿病增加了NTD组大鼠脊髓感觉和运动部分的KIF5B和SYD mRNA以及坐骨神经中的KIF5B含量。此外,运动训练将DT组大鼠的KIF5B和SYD mRNA以及KIF5B含量调节至正常水平。NT组大鼠的运动训练增加了脊髓感觉和运动部分的KIF5B和SYD mRNA以及坐骨神经中的KIF5B含量。
我们的结果表明,糖尿病似乎会改变脊髓KIF5B和SYD mRNA以及坐骨神经KIF5B含量,而运动训练可以对其进行调节,这可能归因于训练引起的高血糖降低。