| 摘要: | 研究背景:
周邊神經損傷引起的神經病理性疼痛使用藥物治療具有不錯的治療效果，但是會產生副作用。運動影響神經病理性疼痛的機轉還不是很清楚。所以本篇研究為了探討運動訓練，一種非藥物治療的方式，是否能提供神經病理性疼痛較佳的治療效果。
材料和方法:
本實驗使用雄性大白鼠接受慢性壓迫性神經損傷建立神經病理性疼痛模式，並且接受運動治療。將所有的雄性大白鼠分成七個組別: 控制組、假手術組、假手術游泳或跑步機運動治療組、神經損傷組、神經損傷游泳或跑步機運動治療組。首先，觀察運動治療後其體重、熱覺過敏和觸覺過敏的變化。並且使用蛋白質轉漬法或酵素連結免疫吸附分析法偵測運動治療後熱休克蛋白72和原發炎細胞介素在坐骨神經的表現量。同時，利用組織病理性檢查法觀察坐骨神經受損接受運動治療後型態學的變化。
結果:
假手術游泳或跑步機運動治療組、神經損傷組、神經損傷游泳或跑步機運動治療組的體重比控制組和假手術組高。一直到手術後第39天，控制組、假手術組、假手術游泳或跑步機運動治療組都沒有發生熱覺過敏和觸覺過敏的現象。神經損傷接收游泳和跑步機運動治療21天後明顯緩解熱覺過敏和觸覺過敏的現象。神經損傷接收游泳和跑步機運動治療22和40天後降低tumor necrosis factor-α和interlukin-1β在坐骨神經的表現量。神經損傷後接受跑步機運動治療22和40天，熱休克蛋白72的表現量增加。
結論:
由以上的研究結果發現游泳和跑步機運動降低熱覺過敏、觸覺過敏、tumor necrosis factor-α和 interlukin-1β的表現。神經損傷後給予跑步機運動治療增加坐骨神經熱休克蛋白72的表現量，但在神經損傷後給予游泳運動治療熱休克蛋白72並無明顯增加。此實驗顯示運動治療能夠提供神經病理性疼痛不錯的治療效果。游泳和跑步機運動治療能夠促進坐骨神經慢性壓迫性損傷後型態學和感覺系統的恢復。
Background: Pharmacotherapies provide an effective efficacy for treatment of neuropathic pain, but they produce side effects. The mechanism of exercise on neuropathic pain is not clear. The aim of this study was to investigate whether exercise training, a non-pharmacotherapy method, provide beneficial effects on neuropathic pain.
Materials and Methods: Male Sprague Dawley rats that suffered for chronic constriction injury (CCI) with/without exercise were used. All rats were divided into 7 groups: control, sham operated, sham operated with swimming or treadmill exercise, CCI, CCI with swimming or treadmill exercise. We observed body weight, thermal hyperalgesia and mechanical allodynia in all groups. The expression of heat shock protein 72 (HSP72) and pro-inflammatory cytokines (tumor necrosis factor-α and interlukin-1β) in sciatic nerve were detected by immunoblotting or ELISA, respectively. We also investigated the morphological change of sciatic nerve after CCI treatment.
Results: The body weight in sham operated with swimming or treadmill exercise, CCI, CCI with swimming or treadmill exercise groups was heavier than that in control and sham operated groups. In control, sham operated, sham operated with swimming or treadmill exercise groups, rats showed no thermal hyperalgesia and mechanical allodynia until day 39 after CCI-treatment. CCI rat with swimming (hyperalgesia, P<0.05; allodynia, P<0.01) or treadmill exercise (hyperalgesia, P<0.05; allodynia, P<0.01) attenuated thermal hyperalgesia and mechanical allodynia significantly, when compared with CCI rats with exercise 21 days after CCI-treatment. We also found that swimming and treadmill exercise reduced tumor necrosis factor-α (TNF-α) and interlukin-1β (IL-1β) expression in sciatic nerve 22 or 40 days after CCI-treatment. HSP72 expression in sciatic nerve increased in CCI with treadmill exercise group (P< 0.05), but not in CCI with swimming exercise group, compared with CCI group 22 or 40 days after CCI-treatment. The morphological improvements seen in sciatic nerve in CCI with treadmill or swimming exercise group, compared with CCI group on 22 or 40 days after CCI-treatment.
Conclusions: This study indicated that swimming and treadmill exercise partially ameliorates thermal hyperalgesia, mechanical allodynia, TNF-α and IL-1β expression in sciatic nerve. Treadmill exercise, but not swimming exercise, increased HSP72 expression in sciatic nerve of CCI with exercise rats, compared with CCI without exercise rats. Both of treatment with swimming and treadmill exercise promotes restoration of morphological and functional properties following CCI. |
