Duchenne muscular dystrophy (DMD) is characterized by progressive muscle necrosis. One of the major challenges for prescribing physical rehabilitation exercises for DMD patients is associated with the lack of a thorough knowledge of dystrophic muscle responsiveness to exercise. This study aims to understand the relationship between myogenic regulation, inflammation and oxidative stress parameters, and disease progression induced by downhill running in the skeletal muscle of an experimental model of DMD. Six-month-old C57BL/10 and C57BL/10-DMD^mdx male mice were distributed into three groups: Control (C), mdx, and mdx + Exercise (mdx + Ex). Animals were trained in a downhill running protocol for seven weeks. The gastrocnemius muscle was subjected to histopathology, muscle regeneration (myoD and myogenin), inflammation (COX-2), oxidative stress (8-OHdG) immunohistochemistry markers, and gene expression (qPCR) of NF-kB and NADP(H)Oxidase 2 (NOX-2) analysis. In the mdx + Ex group, the gastrocnemius muscle showed a higher incidence of endomysial fibrosis and a lower myonecrosis percentage area. Immunohistochemical analysis revealed decreased myogenin immunoexpression in the mdx group, as well as accentuated immunoexpression of nuclear 8-OHdG in both mdx groups and increase in cytoplasmic 8-OHdG only in the mdx + Ex. COX-2 immunoexpression was related to areas of regeneration process and inflammatory infiltrate in the mdx group, while associated with areas of muscle fibrosis in the mdx + Ex. Moreover, the NF-kB gene expression was not influenced by exercise; however, a NAD(P)HOxidase 2 increase was observed. Oxidative stress and oxidative DNA damage play a significant role in the DMD phenotype progression induced by exercise, compromising cellular patterns resulting in increased endomysial fibrosis.

杜氏肌营养不良症 (DMD) 的特征是进行性肌肉坏死。为 DMD 患者开出身体康复锻炼处方的主要挑战之一是缺乏对营养不良性肌肉对运动的反应性的全面了解。本研究旨在了解肌原性调节、炎症和氧化应激参数与 DMD 实验模型骨骼肌中下坡跑步诱导的疾病进展之间的关系。六个月大的 C57BL/10 和 C57BL/10-DMD ^mdx雄性小鼠被分为三组：对照组 (C)、mdx和mdx  + 运动 ( mdx + 例如）。动物接受了为期七周的下坡跑步训练。对腓肠肌进行组织病理学、肌肉再生（myoD 和肌细胞生成素）、炎症 (COX-2)、氧化应激 (8-OHdG) 免疫组织化学标记物以及 NF-kB 和 NADP(H) 氧化酶 2 的基因表达 (qPCR) (NOX-2) 分析。在mdx  +Ex组中，腓肠肌肌内膜纤维化发生率较高，肌坏死面积百分比较低。免疫组织化学分析显示mdx组中肌细胞生成素免疫表达降低，两个mdx组中核 8-OHdG 的免疫表达增强，而细胞质 8-OHdG 仅在mdx中增加 + 例如。COX-2 免疫表达与mdx组中的再生过程和炎症浸润区域相关，而与mdx  + Ex中的肌肉纤维化区域相关。此外，NF-kB基因表达不受运动影响；然而，观察到 NAD(P)HOxidase 2 增加。氧化应激和氧化 DNA 损伤在运动诱导的 DMD 表型进展中起重要作用，损害细胞模式，导致肌内膜纤维化增加。