游泳运动对神经毒素引起的小鼠运动机能损伤的保护作用

Swimming Exercise Enhances Motor Function and Remits MPTP-Induced Motor Abnormalities in PD Mice Model

目的观察游泳运动对神经毒素(MPTP)致小鼠神经和运动机能损伤的保护作用,探讨可能存在的机制。方法在注射MPTP或生理盐水前1d和注射后1、4、7、10d,测量MPTP游泳组、MPTP非游泳组和生理盐水对照组小鼠的爬杆时间和步伐,第11天用放射自显影法测定纹状体多巴胺转运体密度。结果MPTP两组第1天步伐延长,随后恢复。第4天MPTP非游泳组步伐小于生理盐水组和游泳组,后两组差异无显著性。MPTP两组第1天爬杆时间延长,但与生理盐水组比较差异无显著性。游泳组在随后各时间点爬杆时间依次缩短,并在第7、10天明显短于MPTP非游泳组和生理盐水组。游泳组纹状体多巴胺转运体相对密度较非游泳组和生理盐水组明显下调。后两组无差异。结论游泳运动能增强小鼠的运动机能,减轻MPTP的损伤效应,纹状体多巴胺转运体下调可能是其中机制之一。

Objective To investigate MPTP-induced motor disorders and swimming exercise-conferred protection against the neurotoxicity in mice. Methods Four-limb stride length and pole-time were recorded 1 day before and 1,4, 7, 10 days after MPTP or saline injection in MPTP sedentary or MPTP ＋ swim mice and saline controls. Striatal dopamine transporter （DAT） was measured by autoradiography at day 11. Results MPTP induced increase in stride length at day 1 compared with that in saline group showed very significant difference （P ≤ 0. 001 ）. MPTP sedentary group had shorter stride length than that of saline group （ P = 0. 022） and MPTP swimming group （ P = 0. 007）, with no significant difference between the last two groups （ P = 0. 834） at day 4. MPTP increased pole-time at day 1 but not significantly compared with that in saline group （ P = 0.395）. Pole-time was increasingly shortened from day 4 （ P 〉 0.05）, day 7（ P 〈 0.02） to day 10 （ P 〈 0.001 ） in swimming group compared with the other two groups. Striatal DAT relative density （0.63 ± 0.47） was much lower in swimming group than that in lesion in the sedentary group （0.92 ± 0.38, P 〈 0.001） and saline group （0.96 ± 0.41, P 〈 0.001）, with nonsignificant difference between the last two groups （ P = 0. 448 ）. Conclusion Swimming exercise can reinforce murine motor function and alleviate MPTP- related motor disorder, which may oartiallv be induced by the downregulation of striatal DAT.