Borghi Sergio M, Zarpelon Ana C, Pinho-Ribeiro Felipe A, Cardoso Renato D R, Cunha Thiago M, Alves-Filho José C, Ferreira Sergio H, Cunha Fernando Q, Casagrande Rubia, Verri Waldiceu A
Departamento de Patologia, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
J Pharm Pharmacol. 2014 Jul;66(7):1009-20. doi: 10.1111/jphp.12226. Epub 2014 Feb 13.
The role of interleukin (IL)-1β in intense acute swimming-induced muscle mechanical hyperalgesia was investigated in mice.
Untrained mice were submitted to one session of intense acute swimming for 120 min or were submitted to sham conditions (30 s exposure to water), and muscle mechanical hyperalgesia (before and 6-48 h after swimming session), IL-1β production (skeletal muscle and spinal cord), myeloperoxidase activity, reduced glutathione (GSH) levels (skeletal muscle and spinal cord), and cortisol, glucose, lactate and creatine kinase (CK) levels (plasma) were analysed.
Intense acute swimming-induced muscle mechanical hyperalgesia was dose-dependently inhibited by IL-1ra treatment. IL-1β levels were increased in soleus, but not gastrocnemius muscle and spinal cord 2 and 4 h after the session, respectively. Intense acute swimming-induced increase of myeloperoxidase activity and reduced GSH levels in soleus muscle were reversed by IL-1ra treatment. In the spinal cord, exercise induced an increase of GSH levels, which was reduced by IL-1ra. Finally, IL-1ra treatment reduced plasma levels of CK, an indicator of myocyte damage.
IL-1β mediates intense acute swimming-induced muscle mechanical hyperalgesia by peripheral (soleus muscle) and spinal cord integrative mechanisms and could be considered a potential target to treat exercise-induced muscle pain.
研究白细胞介素（IL）-1β在剧烈急性游泳诱导的小鼠肌肉机械性痛觉过敏中的作用。
将未经训练的小鼠进行一次120分钟的剧烈急性游泳，或使其处于假手术条件下（暴露于水中30秒），并分析肌肉机械性痛觉过敏（游泳前后及游泳后6 - 48小时）、IL-1β产生（骨骼肌和脊髓）、髓过氧化物酶活性、还原型谷胱甘肽（GSH）水平（骨骼肌和脊髓）以及皮质醇、葡萄糖、乳酸和肌酸激酶（CK）水平（血浆）。
IL-1受体拮抗剂（IL-1ra）治疗可剂量依赖性地抑制剧烈急性游泳诱导的肌肉机械性痛觉过敏。游泳后2小时和4小时，比目鱼肌中IL-1β水平升高，而腓肠肌和脊髓中未升高。IL-1ra治疗可逆转剧烈急性游泳诱导的比目鱼肌中髓过氧化物酶活性增加和GSH水平降低。在脊髓中，运动诱导GSH水平升高，而IL-1ra可使其降低。最后，IL-1ra治疗降低了血浆CK水平，CK是心肌细胞损伤的指标。
IL-1β通过外周（比目鱼肌）和脊髓整合机制介导剧烈急性游泳诱导的肌肉机械性痛觉过敏，可被视为治疗运动性肌肉疼痛的潜在靶点。
