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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Forced-exercise attenuates experimental autoimmune neuritis
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Forced-exercise attenuates experimental autoimmune neuritis

机译：强迫运动可减轻实验性自身免疫性神经炎

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摘要

Physical inactivity in combination with a sedentary lifestyle is strongly associated with an increased risk of development of inflammatory-mediated diseases, including autoimmune disorders. Recent studies suggest that anti-inflammatory effects of physical exercise may be of therapeutic value in some affected individuals. In this study, we determined the effects of forced-exercise (treadmill running) on the development and progression of experimental autoimmune neuritis (EAN), an established animal model of Guillain-Barré syndrome. Adult male Lewis rats were subjected to sedentary (control) or forced-exercise (1.2 km per day, 5 days a week) for three weeks prior to induction of EAN. P2 (53-78)-immunized sedentary control rats developed a monophasic course of EAN beginning on post-injection day 12.33 ± 0.59 (n = 18) and reaching peak severity on day 15.83 ± 0.35 (n = 18). At near peak of disease, ankle- and sciatic notch-evoked compound muscle action potential (CMAP) amplitudes in sedentary control rats were reduced (～50%) while motor nerve conduction velocity (MNCV) was slowed (～30%) compared with pre-induction evoked responses. In marked contrast, rats undergoing forced-exercise exhibited a significantly less severe clinical course of EAN beginning on post-injection day 12.63 ± 0.53 (n = 16) and reaching peaking severity on day 14.69 ± 0.73 (n = 16). At near peak of disease, ankle- and sciatic-notch-evoked CMAP amplitudes in forced-exercised rats were preserved while EAN-associated slowing of MNCV was modestly attenuated by exercise. Three weeks of forced-exercise reduced by 46% total plasma corticosterone content while elevating the levels of corticosteroid binding globulin. We conclude from this study that forced-exercise administered prior to and during development of EAN affords a novel measure of protection against autoimmune-associated deficits in peripheral nerve evoked responses independent of steroid-induced immune suppression.
机译：缺乏运动和久坐不动的生活方式与发炎性疾病（包括自身免疫性疾病）发展的风险增加密切相关。最近的研究表明，体育锻炼的抗炎作用在某些受影响的个体中可能具有治疗价值。在这项研究中，我们确定了强制锻炼（跑步机）对实验性自身免疫性神经炎（EAN）（已建立的格林-巴利综合征的动物模型）的发育和进展的影响。成年雄性Lewis大鼠在诱导EAN之前要进行久坐（对照）或强迫运动（每天1.2 km，每周5天），持续三周。经P2（53-78）免疫的久坐对照大鼠在注射后第12.33±0.59天（n = 18）开始出现单相EAN发作，并在第15.83±0.35天（n = 18）达到严重程度峰值。与疾病前期相比，久坐对照组大鼠的脚踝和坐骨缺刻诱发的复合肌肉动作电位（CMAP）振幅降低（〜50％），运动神经传导速度（MNCV）减慢（〜30％）。 -诱导诱发的反应。与之形成鲜明对比的是，进行强迫运动的大鼠从注射后第12.63±0.53天（n = 16）开始表现出严重的EAN临床病程，并在第14.69±0.73天（n = 16）达到峰值。在疾病接近高峰时，保留了被强迫锻炼大鼠的踝关节和坐骨神经槽口诱发的CMAP振幅，而运动引起的EAN相关MNCV减慢被减弱。三周的强迫运动使血浆皮质类固醇激素含量降低了46％，同时增加了糖皮质激素结合球蛋白的水平。我们从这项研究中得出结论，在EAN的发展之前和过程中进行强制锻炼可提供一种新的保护措施，以抵抗与类固醇诱导的免疫抑制无关的周围神经引起的反应中自身免疫相关的缺陷。

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