Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling
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...
Saved in:
Main Authors: | , , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
BMC
2024-12-01
|
Series: | Journal of Orthopaedic Surgery and Research |
Subjects: | |
Online Access: | https://doi.org/10.1186/s13018-024-05270-1 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
_version_ | 1841559232322732032 |
---|---|
author | Yingqi Zhang Hanyu Zhang Jiayue Liu Jiawei Sun Yue Xu Narentuya Shi Hongzheng Zhang Jiawang Yan Jinping Chen Hourong Wang Tianyuan Yu |
author_facet | Yingqi Zhang Hanyu Zhang Jiayue Liu Jiawei Sun Yue Xu Narentuya Shi Hongzheng Zhang Jiawang Yan Jinping Chen Hourong Wang Tianyuan Yu |
author_sort | Yingqi Zhang |
collection | DOAJ |
description | 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. |
format | Article |
id | doaj-art-a63d98a30746472a90bdf7ec630d9a7b |
institution | Kabale University |
issn | 1749-799X |
language | English |
publishDate | 2024-12-01 |
publisher | BMC |
record_format | Article |
series | Journal of Orthopaedic Surgery and Research |
spelling | doaj-art-a63d98a30746472a90bdf7ec630d9a7b2025-01-05T12:41:31ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2024-12-0119111010.1186/s13018-024-05270-1Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signalingYingqi Zhang0Hanyu Zhang1Jiayue Liu2Jiawei Sun3Yue Xu4Narentuya Shi5Hongzheng Zhang6Jiawang Yan7Jinping Chen8Hourong Wang9Tianyuan Yu10School of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineDepartment of Acupuncture and Massage, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical SciencesSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese MedicineAbstract 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.https://doi.org/10.1186/s13018-024-05270-1Peripheral nerve injuryTuinaMuscle atrophyMicrocirculationPI3K/AKT pathway |
spellingShingle | Yingqi Zhang Hanyu Zhang Jiayue Liu Jiawei Sun Yue Xu Narentuya Shi Hongzheng Zhang Jiawang Yan Jinping Chen Hourong Wang Tianyuan Yu Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling Journal of Orthopaedic Surgery and Research Peripheral nerve injury Tuina Muscle atrophy Microcirculation PI3K/AKT pathway |
title | Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling |
title_full | Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling |
title_fullStr | Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling |
title_full_unstemmed | Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling |
title_short | Tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of PI3K/Akt signaling |
title_sort | tuina alleviates the muscle atrophy induced by sciatic nerve injury in rats through regulation of pi3k akt signaling |
topic | Peripheral nerve injury Tuina Muscle atrophy Microcirculation PI3K/AKT pathway |
url | https://doi.org/10.1186/s13018-024-05270-1 |
work_keys_str_mv | AT yingqizhang tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT hanyuzhang tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT jiayueliu tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT jiaweisun tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT yuexu tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT narentuyashi tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT hongzhengzhang tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT jiawangyan tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT jinpingchen tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT hourongwang tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling AT tianyuanyu tuinaalleviatesthemuscleatrophyinducedbysciaticnerveinjuryinratsthroughregulationofpi3kaktsignaling |