PDF(Pubmed)
Abstract：
Muscle atrophy due to limb immobilization and inactivity is a common consequence of many diseases and treatment processes. One of the systems activated in inflammatory conditions is the renin-angiotensin system (RAS). The present study was conducted with the aim of investigating the effects of one of the angiotensin-converting enzyme (ACE) inhibitors, enalapril, on improving muscle atrophy caused by immobility. The study was conducted in three groups: a control, an atrophy, and an atrophy group treated with enalapril on Balb/c mice. After tying a splint to cause atrophy in one of the legs, daily treatment with enalapril intraperitoneally (dissolved in DMSO) at a dose of 10 mg/kg/day was done for 7 days. On the eighth day, the splint was opened and half of the mice were evaluated. Then, in the recovery phase, treatment with enalapril was continued in the remaining mice for 10 days without a splint. At the end of each phase, the mice were examined for the muscle strength of the lower limb muscles, and histological and biochemical analyses were subsequently carried out. The tissue level of the oxidative stress index MDA was evaluated, which showed a significantly lower level in the enalapril group compared to the atrophy group (*P<0.1). Also, inflammatory factors in the enalapril group showed a decrease compared to the atrophy group. The strength of four limbs in the mice of the treatment group (-18.36 ± 1.70 %) was significantly higher than that of the atrophy group (-30.33 ± 3 %) at the end of the atrophy phase and also after 10 days of recovery. The results suggest that the use of enalapril that reduces the activation of angiotensin II-dependent pro-oxidant and pro-inflammatory pathways may improve the functional disorder and muscle necrosis in the murine model of muscle atrophy.
摘要：
由于肢体固定和不活动而导致的肌肉萎缩是许多疾病和治疗过程的常见后果。在炎性病症中活化的系统之一是肾素-血管紧张素系统(RAS)。本研究旨在研究一种血管紧张素转换酶（ACE）抑制剂的作用。依那普利,改善不活动引起的肌肉萎缩。该研究分为三组：对照组，萎缩,和用依那普利治疗Balb/c小鼠的萎缩组。系好夹板导致其中一条腿萎缩后，每天以10mg/kg/天的剂量进行依那普利腹膜内治疗（溶解于DMSO中），共7天。第八天,打开夹板并评估一半的小鼠。然后，在恢复阶段，其余小鼠在没有夹板的情况下继续用依那普利治疗10天。在每个阶段结束时,检查小鼠下肢肌肉的肌肉力量，随后进行了组织学和生化分析。评价氧化应激指标MDA的组织水平,与萎缩组相比，依那普利组的水平显着降低（*P<0.1）。此外，与萎缩组相比，依那普利组的炎症因子降低。在萎缩期结束时和恢复10天后，治疗组小鼠的四肢力量（-18.36±1.70％）明显高于萎缩组（-30.33±3％）。结果表明，使用依那普利可以减少血管紧张素II依赖性促氧化剂和促炎途径的激活，可以改善小鼠肌肉萎缩模型中的功能障碍和肌肉坏死。
