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首页> 外文期刊>The Journal of Musculoskeletal and Neuronal Interactions >Comparing effects of rest with or without a NK1RA on fibrosis and sensorimotor declines induced by a voluntary moderate demand task
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Comparing effects of rest with or without a NK1RA on fibrosis and sensorimotor declines induced by a voluntary moderate demand task

机译：比较有或没有NK1RA的休息对自愿性中度需求任务引起的纤维化和感觉运动下降的影响

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Objectives: Fibrosis is one contributing factor in motor dysfunction and discomfort in patients with overusemusculoskeletal disorders. We pharmacologically targeted the primary receptor for Substance P, neurokinin-1, using aspecific antagonist (NK1RA) in a rat model of overuse with the goal of improving tissue fibrosis and discomfort. Methods:Female rats performed a low repetition, high force (LRHF) grasping task for 12 weeks, or performed the task for 12weeks before being placed on a four week rest break, with or without simultaneous NK1RA treatment. Results werecompared to control rats (untreated, or treated 4 weeks with NK1RA or vehicle). Results: Rest improved LRHF-induceddeclines in grip strength, although rest plus NK1RA treatment (Rest /NK1RA) rescued it. Both treatments improvedLRHF-induced increases in muscle TGFβ1 and collagen type 1 levels, forepaw mechanical hypersensitivity (Rest/NK1RAmore effectively), macrophage influx into median nerves, and enhanced collagen deposition in forepaw dermis. Only Rest/NK1RA reduced muscle hypercellularity. However, LRHF+4wk Rest /NK1RA rats showed hyposensitivity to noxious hottemperatures. Conclusions: While the NK1RA induced hot temperature hyposensitivity should be taken into considerationif this or related drug were used long-term, the NK1RA more effectively reduced muscle hypercellularity and improved gripstrength and forepaw mechanical hypersensitivity.
机译：目的：纤维化是过度使用肌肉骨骼疾病患者运动功能障碍和不适的一个促成因素。我们在过度使用的大鼠模型中使用特异性拮抗剂（NK1RA）在药理学上靶向P物质的主要受体Neurokinin-1，目的是改善组织纤维化和不适感。方法：雌性大鼠执行低重复，高力（LRHF）抓握任务持续12周，或执行任务12周，然后再进行四周休息休息，无论是否同时进行NK1RA治疗。将结果与对照大鼠（未治疗或用NK1RA或媒介治疗4周）进行比较。结果：尽管休息加上NK1RA治疗（Rest / NK1RA）得以挽救，休息可以改善LRHF引起的握力下降。两种治疗均改善了LRHF诱导的肌肉TGFβ1和1型胶原蛋白水平的增加，前爪机械性超敏反应（Rest / NK1RA更有效），巨噬细胞向正中神经的流入以及前胶原在真皮中的沉积。只有Rest / NK1RA减少了肌肉细胞过多。然而，LRHF + 4wk Rest / NK1RA大鼠表现出对有害高温的敏感性不足。结论：长期使用NK1RA或相关药物时，应考虑NK1RA引起的热敏感性低下，但NK1RA可更有效地减少肌肉细胞过多，并增强握力和前肢机械性超敏反应。

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