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首页> 外文期刊>Pain. >Regular physical activity prevents chronic pain by altering resident muscle macrophage phenotype and increasing interleukin-10 in mice
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Regular physical activity prevents chronic pain by altering resident muscle macrophage phenotype and increasing interleukin-10 in mice

机译：定期进行体育锻炼可以通过改变小鼠体内的肌肉巨噬细胞表型和增加白介素10来预防慢性疼痛

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Regular physical activity in healthy individuals prevents development of chronic musculoskeletal pain; however, the mechanisms underlying this exercise-induced analgesia are not well understood. Interleukin-10 (IL-10), an antiinflammatory cytokine that can reduce nociceptor sensitization, increases during regular physical activity. Since macrophages play a major role in cytokine production and are present in muscle tissue, we propose that physical activity alters macrophage phenotype to increase IL-10 and prevent chronic pain. Physical activity was induced by allowing C57BL/6J mice free access to running wheels for 8 weeks and compared to sedentary mice with no running wheels. Using immunohistochemical staining of the gastrocnemius muscle to label regulatory (M2, secretes antiinflammatory cytokines) and classical (M1, secretes proinflammatory cytokines) macrophages, the percentage of M2-macrophages increased significantly in physically active mice (68.5% +/- 4.6% of total) compared with sedentary mice (45.8% +/- 7.1% of total). Repeated acid injections into the muscle enhanced mechanical sensitivity of the muscle and paw in sedentary animals, which does not occur in physically active mice; no sex differences occur in either sedentary or physically active mice. Blockade of IL-10 systemically or locally prevented the analgesia in physically active mice, ie, mice developed hyperalgesia. Conversely, sedentary mice pretreated systemically or locally with IL-10 had reduced hyperalgesia after repeated acid injections. Thus, these results suggest that regular physical activity increases the percentage of regulatory macrophages in muscle and that IL-10 is an essential mediator in the analgesia produced by regular physical activity.
机译：健康个体的定期体育锻炼可防止慢性肌肉骨骼疼痛的发展;然而，这种运动引起的镇痛的机制尚不十分清楚。白细胞介素10（IL-10）是一种抗炎细胞因子，可以降低伤害感受器的敏感性，在正常体育锻炼中会增加。由于巨噬细胞在细胞因子的产生中起主要作用，并且存在于肌肉组织中，因此我们提出体育活动会改变巨噬细胞表型，从而增加IL-10并预防慢性疼痛。通过允许C57BL / 6J小鼠自由进入跑步轮8周来诱导体育活动，并与没有跑步轮的久坐小鼠进行比较。使用腓肠肌的免疫组织化学染色标记调节性巨噬细胞（M2，分泌抗炎细胞因子）和经典巨噬细胞（M1，分泌促炎性细胞因子），运动活跃小鼠中M2巨噬细胞的百分比显着增加（占总数的68.5％+/- 4.6％） ）与久坐的老鼠（总数的45.8％+/- 7.1％）相比。反复向肌肉注射酸可增强久坐动物肌肉和爪的机械敏感性，这在运动活跃的小鼠中不会发生;久坐或运动的小鼠均无性别差异。 IL-10的系统性或局部性阻断可预防体育活动小鼠的镇痛作用，即小鼠发展为痛觉过敏。相反，经反复酸注射后，久坐小鼠全身或局部用IL-10预处理可减轻痛觉过敏。因此，这些结果表明，定期进行体育锻炼会增加肌肉中调节性巨噬细胞的百分比，并且IL-10是定期进行体育锻炼所产生的镇痛作用的重要介质。

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