Lim So-Jung, Kim Hyun-Jin, Kim Hansik, Nam Heesoo, Nam Kyung-Soo, Kim Inho, Kang Ryun, Hwang Inyoung, Kang Ju-Seop
Department of Pharmacology, College of Medicine, Hanyang University, Seoul 04763, Republic of Korea.
Department of Physical Education, Graduate School, Korea University, Seoul 02841, Republic of Korea.
Life (Basel). 2025 Mar 21;15(4):517. doi: 10.3390/life15040517.
Muscle atrophy, a physiological decline in muscle mass and strength due in ageing, occurs through an imbalance between protein breakdown and synthesis. The purpose of this study was to verify whether amino acid complex supplementation (ACS) can prevent and treat muscle loss in a dexamethasone (Dexa, 800 μg/kg)-induced rat model of sarcopenia. Sprague Dawley rats (6 weeks old) were assigned to seven groups: (i) normal control, (ii) positive control (high-dose ACS, 500 mg), (iii) Dexa only, (iv) Dexa + high-dose ACS (500 mg), (v) Dexa + medium-dose ACS (300 mg), (vi) Dexa + low-dose ACS (100 mg), or (vii) Dexa + liquid amino acid complex formulation (LF, 2 mL), administered orally for 4 weeks. Exercise capacity tests were performed five times using a treadmill test (TT) and forced swimming test (FST). The body weight increase in each group was less than that of the normal group. The blood biochemical indices, AST levels, and AST/ALT ratio significantly increased in the Dexa-treated medium-dose ACS group. The total muscle protein also significantly increased in all ACS groups. In the Dexa-treated LF group, CK decreased below the normal level. Exercise capacity, assessed by TT and FST, increased the most in the positive control and Dexa-treated high-dose ACS groups. In the TT, the Dexa-only group increased by about 18%, but the Dexa-treated high-dose ACS group increased by about 110%. Additionally, in the FST, Dexa-treated rats receiving a high dose of ACS demonstrated significantly increased exercise time and capacity. Electron microscopic (EM) and hematoxylin and eosin (H&E) observations of muscle tissue revealed muscle fiber atrophy in the gastrocnemius muscles of the Dexa-only group. In the EM findings of the Dexa-treated high-dose ACS group, the M-line and Z-line were clearer than in the Dexa-only group, and the mitochondria were partially preserved. In conclusion, the ACS-treated rats showed a clear recovery from muscle damage based on serum indices, total muscle protein mass, and the microscopic findings on muscle tissue. Notably, a high dose of ACS demonstrated the most effective protection and recovery of muscle tissue in the Dexa-induced sarcopenia rat model.
肌肉萎缩是由于衰老导致肌肉质量和力量的生理性下降，它是由蛋白质分解和合成之间的失衡引起的。本研究的目的是验证补充氨基酸复合物（ACS）是否能预防和治疗地塞米松（Dexa，800μg/kg）诱导的大鼠肌肉减少症模型中的肌肉损失。将6周龄的Sprague Dawley大鼠分为七组：（i）正常对照组，（ii）阳性对照组（高剂量ACS，500mg），（iii）仅地塞米松组，（iv）地塞米松+高剂量ACS（500mg）组，（v）地塞米松+中剂量ACS（300mg）组，（vi）地塞米松+低剂量ACS（100mg）组，或（vii）地塞米松+液体氨基酸复合制剂（LF，2mL）组，口服给药4周。使用跑步机试验（TT）和强迫游泳试验（FST）进行了五次运动能力测试。每组的体重增加均低于正常组。地塞米松处理的中剂量ACS组的血液生化指标、AST水平和AST/ALT比值显著升高。所有ACS组的总肌肉蛋白也显著增加。在地塞米松处理的LF组中，CK降至正常水平以下。通过TT和FST评估的运动能力在阳性对照组和地塞米松处理的高剂量ACS组中增加最多。在TT中，仅地塞米松组增加了约18%，但地塞米松处理的高剂量ACS组增加了约110%。此外，在FST中，接受高剂量ACS的地塞米松处理的大鼠表现出运动时间和能力显著增加。肌肉组织的电子显微镜（EM）和苏木精-伊红（H&E）观察显示，仅地塞米松组的腓肠肌出现肌肉纤维萎缩。在地塞米松处理的高剂量ACS组的EM结果中，M线和Z线比仅地塞米松组更清晰，线粒体部分保留。总之，基于血清指标、总肌肉蛋白质量和肌肉组织的微观发现，ACS处理的大鼠显示出从肌肉损伤中明显恢复。值得注意的是，在Dexa诱导的肌肉减少症大鼠模型中，高剂量的ACS对肌肉组织表现出最有效的保护和恢复作用。
