Chen Guanghua, Huang Yongbin, Huang Chunman, Li Liwei, Pang Jingqun, Li Hongqiang, Zhang Wenxi
Orthopedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang City, China.
Front Vet Sci. 2024 Sep 12;11:1431110. doi: 10.3389/fvets.2024.1431110. eCollection 2024.
The primary objective of this investigation is to establish an animal model that accurately represents skeletal muscle injury as a consequence of decompression sickness. Additionally, this study aims to delineate the potential mechanisms underlying the development and progression of skeletal muscle damage associated with decompression sickness.
(1) In this research, rats were utilized as experimental models and subjected to 600 kPa pressure in an air medium for a duration of 60 min, followed by decompression at a consistent rate of 1.5 min to reach atmospheric pressure in order to establish an animal model for decompression injury. Assessment of decompression injury involved the observation of general symptoms and signs, as well as histopathological examination of lung tissue to determine the extent of damage in the pulmonary system of rats. (2) Building on the rat decompression injury model, we conducted pathological and serological examinations to assess the status of rat skeletal muscle. Additionally, we investigated the signaling mechanism of the TLR9-MyD88 pathway in mediating alterations in rat skeletal muscle resulting from decompression injury, and evaluated the effects of decompression injury on apoptosis in rat skeletal muscle.
Repeated decompression induces significant damage to skeletal muscle tissue, characterized by edema, fiber rupture, and atrophy. This process also leads to a transient elevation in creatine kinase (CK-MM) levels in rat serum, as well as an upregulation of proteins such as TLR9, MyD88, p38, and ERK in rat skeletal muscle tissue. Furthermore, repeated decompression results in a temporary increase in the transcription levels of Atrogen-1mRNA and MuRF-1mRNA in rat skeletal muscle tissue.
The decompression protocol applied in this study successfully induced decompression sickness in a rat model, leading to skeletal muscle damage that was consistent with the expected pathology of decompression injury. Despite the initial injury, the rats showed evidence of adaptation following prolonged exposure to decompression conditions.
本研究的主要目的是建立一种能准确模拟减压病所致骨骼肌损伤的动物模型。此外，本研究旨在阐明与减压病相关的骨骼肌损伤发生和发展的潜在机制。
（1）在本研究中，将大鼠用作实验模型，在空气介质中使其承受600kPa的压力持续60分钟，然后以1.5分钟的恒定速率减压至大气压，以建立减压损伤动物模型。减压损伤的评估包括观察一般症状和体征，以及对肺组织进行组织病理学检查以确定大鼠肺部系统的损伤程度。（2）在大鼠减压损伤模型的基础上，我们进行了病理和血清学检查以评估大鼠骨骼肌的状态。此外，我们研究了TLR9-MyD88途径在介导减压损伤导致的大鼠骨骼肌变化中的信号传导机制，并评估了减压损伤对大鼠骨骼肌细胞凋亡的影响。
反复减压会导致骨骼肌组织出现明显损伤，其特征为水肿、纤维断裂和萎缩。这一过程还会导致大鼠血清中肌酸激酶（CK-MM）水平短暂升高，以及大鼠骨骼肌组织中TLR9、MyD88、p38和ERK等蛋白质上调。此外，反复减压会导致大鼠骨骼肌组织中Atrogen-1mRNA和MuRF-1mRNA的转录水平暂时升高。
本研究中应用的减压方案在大鼠模型中成功诱发了减压病，导致骨骼肌损伤，与预期的减压损伤病理学一致。尽管有初始损伤，但大鼠在长时间暴露于减压条件后显示出适应的迹象。
