中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (8): 714-722.doi: 10.3969/j.issn.1673-5374.2013.08.006

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

长期运动训练与力竭运动：谁能降低染铅大鼠的神经毒性

  

  • 收稿日期:2012-10-08 修回日期:2013-01-05 出版日期:2013-03-15 发布日期:2013-03-15

Chronic exercise training versus acute endurance exercise in reducing neurotoxicity in rats exposed to lead acetate

Mohammad Shahandeh1, Valiollah Dabidi Roshan2, Somayeh Hosseinzadeh3, Soleiman Mahjoub4, Vaginak Sarkisian1   

  1. 1 L.Orbeli Inst. of Physiology, NAS of Armenia, Yerevan, Republic of Armenia
    2 College of Physical Education and Sport Sciences, Department of Sport Physiology, University of Mazandaran, Babolsar, Iran
    3 Babol University of Medical Sciences, Babol, Iran
    4 Department of Biochemistry and Biophysics, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran
  • Received:2012-10-08 Revised:2013-01-05 Online:2013-03-15 Published:2013-03-15
  • Contact: Somayeh Hosseinzadeh, M.Sc, Babol University of Medical Sciences, Babol, Iran, hoseinzadeh87@ yahoo.com.
  • About author:Mohammad Shahandeh☆, Studying for doctorate.

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摘要：

大鼠腹腔注射20 mg/kg醋酸铅进行铅暴露干预后，分别接受8周(15-22 m/min, 25-64 min)平板跑步的长期运动训练或/和1.6 km/h平板跑步直至力竭的急性训练。铅暴露大鼠海马脑源性神经营养因子含量下降不明显，但血浆总抗氧化能力明显降低，海马和血浆丙二醛水平明显提高。8周的长期运动训练使染铅大鼠海马脑源性神经营养因子含量和血浆总抗氧化能力明显上升，血浆丙二醛水平明显下降。急性力竭运动只提高染铅大鼠血浆丙二醛水平，长期运动训练联合力竭运动明显降低染铅大鼠总抗氧化能力。说明运动量较小的长期运动训练可明显减轻铅暴露的神经毒性作用，减轻机体氧化应激，而急性力竭运动则无这些正性作用。

关键词: 神经再生, 神经康复, 生物因子, 长期运动训练, 力竭运动, 平板训练, 铅, 铅中毒, 神经毒性, 氧化应激, 海马, 脑源性神经营养因子

Abstract:

After intraperitoneal injection of 20 mg/kg lead acetate, rats received 8 weeks of treadmill exercise (15–22 m/min, 25–64 minutes) and/or treadmill exercise at 1.6 km/h until exhaustion. The markers related to neurotoxicity were measured by enzyme-linked immunosorbent assay method. 8 weeks of treadmill exercise significantly increased brain-derived neurotrophic factor level in the hippocampus (P = 0.04) and plasma level of total antioxidant capacity of rats exposed to lead acetate (P < 0.001), and significantly decreased plasma level of malondialdehyde (P < 0.001). Acute exercise only decreased the hippocampal malondialdehyde level (P = 0.09) and increased brain-derived neurotrophic factor level in the hippocampus (P = 0.66). Acute exercise also enhanced the total antioxidant capacity in rats exposed to lead acetate, insignificantly (P = 0.99). These findings suggest that chronic treadmill exercise can significantly decrease neurotoxicity and alleviate oxidative stress in rats exposed to lead acetate. However, acute endurance exercise was not associated with these beneficial effects.

Key words: neural regeneration, neurorehabilitation, long-term exercise training, endurance exercise, treadmill, lead poisoning, neurotoxicity, oxidative stress, hippocampus, brain-derived neurotrophic factor, neuroregeneration