1. Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling.
- Author
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Zhang Y, Zhang H, Liu J, Sun J, Xu Y, Shi N, Zhang H, Yan J, Chen J, Wang H, and Yu T
- Subjects
- Animals, Male, Rats, Sciatic Nerve injuries, Insulin-Like Growth Factor I metabolism, Disease Models, Animal, Peripheral Nerve Injuries metabolism, Muscular Atrophy etiology, Muscular Atrophy metabolism, Muscular Atrophy pathology, Proto-Oncogene Proteins c-akt metabolism, Signal Transduction physiology, Phosphatidylinositol 3-Kinases metabolism, Rats, Sprague-Dawley
- 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., Competing Interests: Declarations. Ethical approval and consent to participate: The experimental designs and animal care were approved by the Ethics Committee for Animal Care and Use Committee of the Beijing University of Chinese Medicine (No. BUCM-2023032303-1119), and all procedures were conducted in strict accordance with the National Institutes of Health standards stated in the Guide for the Care and Use of Laboratory Animals. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)
- Published
- 2024
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