Exercise induced myelin protein zero improvement in neuropathic pain rats.

IF 1.3 4区 医学 Q4 NEUROSCIENCES
Somatosensory and Motor Research Pub Date : 2023-12-01 Epub Date: 2023-01-11 DOI:10.1080/08990220.2022.2158800
Ali Ghanbari, Sahar Ghasemi, Sam Zarbakhsh
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引用次数: 0

Abstract

Purpose: Aerobic exercise including swimming plays a suitable role in improving somatosensory injuries. Neuropathic pain is a debilitating condition that occurs following injury or diseases of somatosensory system. In the present study, we tried to investigate the effect of exercise on myelin protein zero of sciatic nerve injured rats.

Materials and methods: Forty male rats (180-220 g) were divided into five groups (intact, sham, sham + exercise, neuropathy, and neuropathy + exercise). Right Sciatic nerve of anesthetized rats was exposed and loosely ligated (four ligations with 1 mm apart) using catgut chromic sutures to induce neuropathy. After 3 days of recovery, swimming exercise began (20 min/day/5 days a week/4 weeks). Mechanical allodynia and thermal hyperalgesia were detected using Von Frey filaments and plantar test, respectively. Sciatic nerve at the place of injury was dissected out to measure the myelin protein zero by western blot analysis. In the intact and sham groups, sciatic nerve removed at the place similar to injured group.

Results: We found that neuropathy significantly (p < 0.05) reduced paw withdrawal mechanical and thermal thresholds and swimming exercise significantly (p < 0.05) increased paw withdrawal mechanical and thermal thresholds compared to the neuropathy group. Moreover, we found that MPZ level significantly (p < 0.01) decreased in neuropathy group against that in sham group, and exercise prominently (p < 0.05) reversed MPZ level towards control level.

Conclusions: Swimming exercise improves myelin protein zero level in neuropathic rats along with attenuating neuropathic pain. This is a promising approach in improving neuropathological disorders including Charcot-Marie-Tooth and Dejerine-Sottas disease.

运动诱导神经性疼痛大鼠髓磷脂蛋白零改善。
目的:包括游泳在内的有氧运动对躯体感觉损伤有一定的改善作用。神经性疼痛是躯体感觉系统损伤或疾病后出现的一种衰弱状态。本研究旨在探讨运动对坐骨神经损伤大鼠髓鞘蛋白0的影响。材料与方法:雄性大鼠40只(180 ~ 220 g)分为5组(完整组、假手术组、假手术+运动组、神经病变组、神经病变+运动组)。麻醉大鼠右侧坐骨神经暴露后,采用线色缝合线松散结扎(4根,间隔1mm),诱导神经病变。恢复3天后开始游泳运动(20分钟/天/每周5天/4周)。采用Von Frey细丝法和足底法分别检测机械异常性痛和热痛觉过敏。解剖损伤部位的坐骨神经,用western blot法测定髓鞘蛋白0。完整组和假手术组坐骨神经切除位置与损伤组相似。结果:我们发现神经病变明显(p p p p p)。结论:游泳运动可提高神经病变大鼠髓鞘蛋白0水平,减轻神经性疼痛。这是一种有希望改善神经病理疾病的方法,包括Charcot-Marie-Tooth病和Dejerine-Sottas病。
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来源期刊
Somatosensory and Motor Research
Somatosensory and Motor Research 医学-神经科学
自引率
0.00%
发文量
4
审稿时长
>12 weeks
期刊介绍: Somatosensory & Motor Research publishes original, high-quality papers that encompass the entire range of investigations related to the neural bases for somatic sensation, somatic motor function, somatic motor integration, and modeling thereof. Comprising anatomical, physiological, biochemical, pharmacological, behavioural, and psychophysical studies, Somatosensory & Motor Research covers all facets of the peripheral and central processes underlying cutaneous sensation, and includes studies relating to afferent and efferent mechanisms of deep structures (e.g., viscera, muscle). Studies of motor systems at all levels of the neuraxis are covered, but reports restricted to non-neural aspects of muscle generally would belong in other journals.
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