Zhang Yingqi, Zhang Hanyu, Liu Jiayue, Sun Jiawei, Xu Yue, Shi Narentuya, Zhang Hongzheng, Yan Jiawang, Chen Jinping, Wang Hourong, Yu Tianyuan
School of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, 100029, People's Republic of China.
Department of Acupuncture and Massage, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, 100730, People's Republic of China.
J Orthop Surg Res. 2024 Dec 31;19(1):892. doi: 10.1186/s13018-024-05270-1.
Tuina is an effective treatment for the decrease of skeletal muscle atrophy after peripheral nerve injury. However, the underlying mechanism of action remains unclear. This study aimed to explore the underlying mechanisms of tuina in rats with sciatic nerve injury (SNI).
We established an SNI rat model. After Tuina intervention, curative effects were evaluated by behavioral assessment, nerve function index, and muscle atrophy index (MAI). Pathological changes were observed by transmission electron microscopy and immunofluorescence. Insulin-like growth factor 1 (IGF-1), forkhead box O (FoxO) and p-FoxO levels were detected using enzyme-linked immunosorbent assay. Western blotting was performed to detect the expression of proteins involved in the PI3K/AKT signaling pathway.
Behavioral assessment, nerve function index, and MAI revealed that the tuina had significantly improved muscle atrophy after SNI compared with the SNI model group. Transmission electron microscopy showed that tuina improved muscle ultramicrostructure. CD31 immunofluorescence revealed that tuina improved microcirculation. Furthermore, we observed that tuina differentially regulated the levels of IGF-1, FoxO and p-FoxO, and the protein expression of p-Phosphoinositide 3-kinase (p-PI3K), p-AKT, and vascular endothelial growth factor in the anterior tibial muscle and soleus muscles.
Tuina could effectively inhibit skeletal muscle atrophy via the microcirculation pathway in a rat model of SNI by regulating the expression of IGF-1 and FoxO. The underlying mechanism of action may involve the PI3K/Akt signaling pathway.
推拿是治疗周围神经损伤后骨骼肌萎缩的有效方法。然而，其潜在作用机制尚不清楚。本研究旨在探讨推拿对坐骨神经损伤（SNI）大鼠的潜在作用机制。
建立SNI大鼠模型。推拿干预后，通过行为学评估、神经功能指数和肌肉萎缩指数（MAI）评估疗效。通过透射电子显微镜和免疫荧光观察病理变化。采用酶联免疫吸附测定法检测胰岛素样生长因子1（IGF-1）、叉头框O（FoxO）和p-FoxO水平。进行蛋白质印迹法检测PI3K/AKT信号通路相关蛋白的表达。
行为学评估、神经功能指数和MAI显示，与SNI模型组相比，推拿显著改善了SNI后的肌肉萎缩。透射电子显微镜显示推拿改善了肌肉超微结构。CD31免疫荧光显示推拿改善了微循环。此外，我们观察到推拿对胫前肌和比目鱼肌中IGF-1、FoxO和p-FoxO的水平以及p-磷酸肌醇3激酶（p-PI3K）、p-AKT和血管内皮生长因子的蛋白表达有不同的调节作用。
在SNI大鼠模型中，推拿可通过调节IGF-1和FoxO的表达，经微循环途径有效抑制骨骼肌萎缩。其潜在作用机制可能涉及PI3K/Akt信号通路。
