Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling.

IF 2.8 3区 医学 Q1 ORTHOPEDICS
Yingqi Zhang, Hanyu Zhang, Jiayue Liu, Jiawei Sun, Yue Xu, Narentuya Shi, Hongzheng Zhang, Jiawang Yan, Jinping Chen, Hourong Wang, Tianyuan Yu
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引用次数: 0

Abstract

Background: 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).

Methods: 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.

Result: 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.

Conclusion: 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.

推拿通过调节PI3K/Akt信号通路减轻大鼠坐骨神经损伤所致的肌肉萎缩。
背景:推拿是减轻周围神经损伤后骨骼肌萎缩的有效治疗方法。然而,其潜在的作用机制尚不清楚。本研究旨在探讨推拿对大鼠坐骨神经损伤(SNI)的作用机制。方法:建立SNI大鼠模型。推拿干预后,采用行为评价、神经功能指数、肌萎缩指数(MAI)评价疗效。透射电镜和免疫荧光观察病理改变。采用酶联免疫吸附法检测胰岛素样生长因子1 (IGF-1)、叉头盒O (FoxO)和p-FoxO水平。Western blotting检测PI3K/AKT信号通路相关蛋白的表达。结果:行为学评估、神经功能指数、MAI显示,与SNI模型组比较,针刺组明显改善SNI后肌肉萎缩。透射电镜显示,推拿可改善肌肉超微结构。CD31免疫荧光显示推拿可改善微循环。此外,我们观察到推拿对胫骨前肌和比目鱼肌中IGF-1、FoxO和p-FoxO的水平以及p-磷酸肌苷激酶(p-PI3K)、p-AKT和血管内皮生长因子的蛋白表达有差异。结论:推拿可通过调节IGF-1和FoxO的表达,通过微循环途径有效抑制SNI模型大鼠骨骼肌萎缩。潜在的作用机制可能涉及PI3K/Akt信号通路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
4.10
自引率
7.70%
发文量
494
审稿时长
>12 weeks
期刊介绍: Journal of Orthopaedic Surgery and Research is an open access journal that encompasses all aspects of clinical and basic research studies related to musculoskeletal issues. Orthopaedic research is conducted at clinical and basic science levels. With the advancement of new technologies and the increasing expectation and demand from doctors and patients, we are witnessing an enormous growth in clinical orthopaedic research, particularly in the fields of traumatology, spinal surgery, joint replacement, sports medicine, musculoskeletal tumour management, hand microsurgery, foot and ankle surgery, paediatric orthopaedic, and orthopaedic rehabilitation. The involvement of basic science ranges from molecular, cellular, structural and functional perspectives to tissue engineering, gait analysis, automation and robotic surgery. Implant and biomaterial designs are new disciplines that complement clinical applications. JOSR encourages the publication of multidisciplinary research with collaboration amongst clinicians and scientists from different disciplines, which will be the trend in the coming decades.
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