4.6 Article

Histopathological changes and oxidative damage in type I and type II muscle fibers in rats undergoing paradoxical sleep deprivation

期刊

CELLULAR SIGNALLING
卷 81, 期 -, 页码 -

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2021.109939

关键词

Sleep deprivation; Muscle atrophy; Oxidative stress

资金

  1. FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) [2013/00152-5, 2018/15921-8]
  2. CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior)
  3. CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) [310276/2017-9, 306138/2017-4]
  4. Associacao Fundo de Incentivo a Pesquisa (AFIP)

向作者/读者索取更多资源

Previous studies have shown that muscle atrophy can be observed after sleep deprivation, but the exact mechanisms are not fully understood. Different types of muscle fibers exhibit variations in oxidative damage and histopathological changes. Muscle predominantly composed of type I fibers show greater oxidative damage and catabolic activity.
Background: previous studies have shown that muscle atrophy is observed after sleep deprivation (SD) protocols; however, the mechanisms responsible are not fully understood. Muscle trophism can be modulated by several factors, including energy balance (positive or negative), nutritional status, oxidative stress, the level of physical activity, and disuse. The metabolic differences that exist in different types of muscle fiber may also be the result of different adaptive responses. To better understand these mechanisms, we evaluated markers of oxidative damage and histopathological changes in different types of muscle fibers in sleep-deprived rats. Methods: Twenty male Wistar EPM-1 rats were randomly allocated in two groups: a control group (CTL group; n = 10) and a sleep deprived group (SD group; n = 10). The SD group was submitted to continuous paradoxical SD for 96 h; the soleus (type I fibers) and plantar (type II fiber) muscles were analyzed for histopathological changes, trophism, lysosomal activity, and oxidative damage. Oxidative damage was assessed by lipid peroxidation and nuclear labeling of 8-OHdG. Results: The data demonstrated that SD increased the nuclear labeling of 8-OHdG and induced histopathological changes in both muscles, being more evident in the soleus muscle. In the type I fibers there was signs of tissue degeneration, inflammatory infiltrate and tissue edema. Muscle atrophy was observed in both muscles. The concentration of malondialdehyde, and cathepsin L activity only increased in type I fibers after SD. Conclusion: These data indicate that the histopathological changes observed after 96 h of SD in the skeletal muscle occur by different processes, according to the type of muscle fiber, with muscles predominantly composed of type I fibers undergoing greater oxidative damage and catabolic activity, as evidenced by a larger increase in 8-OHdG labeling, lipid peroxidation, and lysosomal activity.

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