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低强度长期有氧运动对杜氏肌营养不良症小鼠腰大肌的影响:一种实验模型。

Effects of Low-Intensity and Long-Term Aerobic Exercise on the Psoas Muscle of Mice: An Experimental Model of Duchenne Muscular Dystrophy.

机构信息

Department of Physiological Sciences, Federal University of São Carlos (UFSCar), Rod. Washington Luís, km 235-SP-310-São Carlos, São Paulo 13565-905, Brazil.

Department of Neurosciences and Behaviour, Ribeirão Preto Medical School, University of São Paulo-Ribeirão Preto, São Paulo 14051-160, Brazil.

出版信息

Int J Mol Sci. 2022 Apr 19;23(9):4483. doi: 10.3390/ijms23094483.

Abstract

Duchenne muscular dystrophy (DMD) is a muscle disease characterized by the absence of the protein dystrophin, which causes a loss of sarcolemma integrity, determining recurrent muscle injuries, decrease in muscle function, and progressive degeneration. Currently, there is a need for therapeutic treatments to improve the quality of life of DMD patients. Here, we investigated the effects of a low-intensity aerobic training (37 sessions) on satellite cells, peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α protein (PGC-1α), and different types of fibers of the psoas muscle from mice (DMD experimental model). Wildtype and mice were randomly divided into sedentary and trained groups ( = 24). Trained animals were subjected to 37 sessions of low-intensity running on a motorized treadmill. Subsequently, the psoas muscle was excised and analyzed by immunofluorescence for dystrophin, satellite cells, myosin heavy chain (MHC), and PGC-1α content. The minimal Feret's diameters of the fibers were measured, and light microscopy was applied to observe general morphological features of the muscles. The training (37 sessions) improved morphological features in muscles from mice and caused an increase in the number of quiescent/activated satellite cells. It also increased the content of PGC-1α in the group. We concluded that low-intensity aerobic exercise (37 sessions) was able to reverse deleterious changes determined by DMD.

摘要

杜氏肌营养不良症(DMD)是一种肌肉疾病,其特征是缺乏肌营养不良蛋白,导致肌细胞膜完整性丧失,从而导致反复的肌肉损伤、肌肉功能下降和进行性退化。目前,需要治疗方法来改善 DMD 患者的生活质量。在这里,我们研究了低强度有氧运动(37 次)对卫星细胞、过氧化物酶体增殖物激活受体-γ共激活因子(PGC)-1α蛋白(PGC-1α)和比目鱼肌不同类型纤维的影响, (DMD 实验模型)。野生型和 小鼠被随机分为久坐和训练组( = 24)。训练动物在电动跑步机上进行 37 次低强度跑步。随后,切除比目鱼肌并通过免疫荧光分析肌营养不良蛋白、卫星细胞、肌球蛋白重链(MHC)和 PGC-1α含量。测量纤维的最小 Feret 直径,并应用光镜观察肌肉的一般形态特征。训练(37 次)改善了 小鼠肌肉的形态特征,并增加了静止/激活卫星细胞的数量。它还增加了 组中 PGC-1α的含量。我们得出结论,低强度有氧运动(37 次)能够逆转 DMD 引起的有害变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f876/9105402/4239d4f553d5/ijms-23-04483-g001.jpg

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