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超短波透热疗法对兔模型肌源性挛缩的预防作用及可能机制。

Preventive effect and possible mechanisms of ultrashort wave diathermy on myogenic contracture in a rabbit model.

机构信息

Department of Rehabilitation Medicine, 533251The Second Hospital of Anhui Medical University, Hefei, Anhui, China.

Department of Rehabilitation Medicine, Anhui No.2 Provincial People's Hospital, Hefei, Anhui, China.

出版信息

Sci Prog. 2021 Oct;104(4):368504211054992. doi: 10.1177/00368504211054992.

DOI:10.1177/00368504211054992
PMID:34825614
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10450593/
Abstract

The purpose of this study was to determine the preventive effect of ultrashort wave diathermy on immobilization-induced myogenic contracture and to explore its underlying mechanisms. Forty-two rabbits were randomly assigned into control (Group C), immobilization (Group I, which was further divided into one week, Group I-1; two weeks, Group I-2; and four weeks, Group I-4, subgroups by the length of immobilization) and ultrashort wave prevention (Group U, which was further divided into one week, Group U-1; two weeks, Group U-2; and four weeks, Group U-4, by time of treatment) groups. Intervention effects were assessed by evaluating rectus femoris cross-sectional area (CSA), knee range of motion, and the protein levels for myogenic differentiation (MyoD) and muscle atrophy F-box (MAFbx-1) in the rectus femoris. Compared with those of Group C, in Groups I and U, total contracture, myogenic contracture, MyoD and MAFbx-1 levels were significantly elevated, and CSA was significantly smaller ( < 0.05). Compared with those of Group I at each time point, MyoD levels were significantly elevated, MAFbx-1 levels were significantly lower, CSA was significantly larger, and myogenic contracture was significantly alleviated in Group U ( < 0.05). In the early stages of contracture, ultrashort wave diathermy reduces muscle atrophy and delays the process of myogenic contracture during joint immobilization; the mechanism of this may be explained as increased expression of MyoD triggered by suppression of the MAFbx-1-mediated ubiquitin-proteasome pathway.

摘要

本研究旨在确定超短波透热疗法对固定性肌源性挛缩的预防作用,并探讨其潜在机制。42 只兔子被随机分为对照组(C 组)、固定组(I 组,进一步分为 1 周组(I-1 组)、2 周组(I-2 组)和 4 周组(I-4 组),按固定时间分组)和超短波预防组(U 组,进一步分为 1 周组(U-1 组)、2 周组(U-2 组)和 4 周组(U-4 组),按治疗时间分组)。通过评估股直肌横截面积(CSA)、膝关节活动范围以及股直肌肌源性分化(MyoD)和肌肉萎缩 F 盒(MAFbx-1)的蛋白水平来评估干预效果。与 C 组相比,I 组和 U 组的总挛缩、肌源性挛缩、MyoD 和 MAFbx-1 水平显著升高,CSA 显著减小(<0.05)。与每个时间点的 I 组相比,U 组的 MyoD 水平显著升高,MAFbx-1 水平显著降低,CSA 显著增大,肌源性挛缩显著缓解(<0.05)。在挛缩的早期阶段,超短波透热疗法可减少肌肉萎缩并延缓关节固定过程中的肌源性挛缩;其机制可能是通过抑制 MAFbx-1 介导的泛素-蛋白酶体途径来增加 MyoD 的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/e4b56403d95e/10.1177_00368504211054992-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/a1d5ba59e46a/10.1177_00368504211054992-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/5be203ce4de3/10.1177_00368504211054992-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/a6de172325ae/10.1177_00368504211054992-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/6ad35cedc59b/10.1177_00368504211054992-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/6141ab0392fe/10.1177_00368504211054992-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/e4b56403d95e/10.1177_00368504211054992-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/a1d5ba59e46a/10.1177_00368504211054992-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/5be203ce4de3/10.1177_00368504211054992-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/a6de172325ae/10.1177_00368504211054992-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/6ad35cedc59b/10.1177_00368504211054992-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/6141ab0392fe/10.1177_00368504211054992-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce0f/10450593/e4b56403d95e/10.1177_00368504211054992-fig6.jpg

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