基于 F344xBN 大鼠衰老模型的氯沙坦治疗肌少症的疗效研究。
Study of Therapeutic Effects of Losartan for Sarcopenia Based on the F344xBN Rat Aging Model.
机构信息
Department of life Science, College of BioNano Technology, Gachon University, Gyeonggi-do, Republic of Korea.
Department of Rehabilitation Medicine, Gachon University, Gil Medical Center Incheon, Incheon, Republic of Korea.
出版信息
In Vivo. 2022 Nov-Dec;36(6):2740-2750. doi: 10.21873/invivo.13010.
BACKGROUND/AIM: Sarcopenia is an age-related disease in which muscle mass and strength are markedly reduced. There are few effective treatments, but the angiotensin II receptor antagonist losartan has been reported to be effective. Our aim was to evaluate the therapeutic effectiveness of losartan for sarcopenia and explore the underlying mechanisms.
MATERIALS AND METHODS
We investigated body weight, muscle mass (gastrocnemius, soleus, peroneus longus, and tibialis anterior muscles), and serum markers in an aged rat model population divided into four treatment groups: Control, exercise, losartan, and exercise plus losartan. The rats were sacrificed at 6, 12, or 18 months after the start of the experiment and autopsies were performed.
RESULTS
Compared with the control group, average muscle mass and weight increased in the two groups treated with losartan. AKT serine/threonine kinase (AKT) and extracellular signal-regulated kinase (ERK) muscle growth factors increased in the peroneus longus. mechanistic target of rapamycin kinase (mTOR) increased in tibialis anterior, peroneus longus, and soleus.
CONCLUSION
Losartan treatment slowed muscle degeneration and activated the PI3K-AKT-mTOR and ERK/mitogen-activated protein kinase signalling pathways required for production of muscle growth factors when combined with exercise.
背景/目的：肌少症是一种与年龄相关的疾病，其特征是肌肉质量和力量明显下降。目前治疗方法有限，但有报道称血管紧张素 II 受体拮抗剂氯沙坦可能有效。本研究旨在评估氯沙坦治疗肌少症的疗效，并探讨其潜在机制。
材料和方法
我们在一个分为四个治疗组的老年大鼠模型中研究了体重、肌肉质量（腓肠肌、比目鱼肌、跖肌和胫骨前肌）和血清标志物：对照组、运动组、氯沙坦组和运动加氯沙坦组。实验开始后 6、12 或 18 个月处死大鼠并进行尸检。
结果
与对照组相比，接受氯沙坦治疗的两组大鼠的平均肌肉质量和体重均增加。腓肠肌中 AKT 丝氨酸/苏氨酸激酶（AKT）和细胞外信号调节激酶（ERK）肌肉生长因子增加。胫骨前肌、腓肠肌和比目鱼肌中雷帕霉素靶蛋白激酶（mTOR）增加。
结论
氯沙坦治疗可减缓肌肉退化，并与运动结合激活 PI3K-AKT-mTOR 和 ERK/丝裂原激活蛋白激酶信号通路，促进肌肉生长因子的产生。
Zotero 插件