Joukar Siyavash, Vahidi Reza, Farsinejad Alireza, Asadi-Shekaari Majid, Shahouzehi Beydolah
Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Neurotox Res. 2017 Jul;32(1):41-49. doi: 10.1007/s12640-017-9705-1. Epub 2017 Jan 31.
Despite the importance of this issue, less has been paid to the influence of exercise on the neural side effects of anabolic androgenic steroids and mechanisms. We investigated the effects of two levels of endurance exercise on neurodegeneration side effects of nandrolone. The study period was 8 weeks. Wistar rats were divided into nine groups including the control (CTL) group, mild exercise (mEx) group, and vehicle (Arach) group which received arachis oil intramuscularly, nandrolone (Nan) group which received nandrolone decanoate 5 mg/kg two times weekly, mEx+Arach group which treated with arachis oil along with mild exercise, mEx+Nan group which treated with nandrolone along with mild exercise, severe exercise (sEx) group, sEx+Arach, and sEx+Nan groups. Finally, brain samples were taken for histopathological, biochemical, and western blot analysis. Nandrolone significantly decreased the intact cells of the hippocampus, total antioxidant capacity (TAC) (P < 0.05 versus CTL and Arach groups), TAC to malondialdehyde ratio (TAC/MDA), and Bcl-2. Nandrolone increased the Bax/Bcl-2 ratio of the brain tissue (P < 0.01 versus CTL and Arach groups). Combination of mild exercise and nandrolone rescued the intact cells to some extent, and this effect was associated with the improvement of Bcl-2 level and Bax/Bcl-2 ratio of brain tissue. Combination of severe exercise and nandrolone rescued the intact cells and improved the TAC, TAC/MDA, and Bax/Bcl-2 ratios. The findings suggest that low- and high-intensity endurance exercise decreased the risk of neurodegeneration effect of nandrolone in the hippocampus of rats. This effect can be explained by the regulation of the redox system and cell homeostasis.
尽管这个问题很重要,但关于运动对合成代谢雄激素类固醇神经副作用及其机制的影响却鲜有研究。我们研究了两种耐力运动水平对诺龙神经退行性副作用的影响。研究为期8周。将Wistar大鼠分为九组,包括对照组(CTL)、轻度运动组(mEx)、肌肉注射花生油的赋形剂组(Arach)、每周两次接受5mg/kg癸酸诺龙的诺龙组(Nan)、接受花生油并进行轻度运动的mEx+Arach组、接受诺龙并进行轻度运动的mEx+Nan组、重度运动组(sEx)、sEx+Arach组和sEx+Nan组。最后,采集脑样本进行组织病理学、生化和蛋白质印迹分析。诺龙显著降低了海马体的完整细胞数量、总抗氧化能力(TAC)(与CTL组和Arach组相比,P<0.05)、TAC与丙二醛的比值(TAC/MDA)以及Bcl-2水平。诺龙增加了脑组织的Bax/Bcl-2比值(与CTL组和Arach组相比,P<0.01)。轻度运动与诺龙联合使用在一定程度上挽救了完整细胞,这种效果与脑组织Bcl-2水平和Bax/Bcl-2比值的改善有关。重度运动与诺龙联合使用挽救了完整细胞,并改善了TAC、TAC/MDA和Bax/Bcl-2比值。研究结果表明,低强度和高强度耐力运动降低了诺龙对大鼠海马体神经退行性影响的风险。这种效果可以通过氧化还原系统和细胞稳态的调节来解释。