4.5 Article

Physical Training Protects Against Brain Toxicity in Mice Exposed to an Experimental Model of Glioblastoma

期刊

NEUROCHEMICAL RESEARCH
卷 47, 期 11, 页码 3344-3354

出版社

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-022-03685-y

关键词

Physical exercise; Glioblastoma; Oxidative stress; Inflammation; Brain tumor

资金

  1. Coordination for the Improvement of Higher Education Personnel (CAPES/BRAZIL)
  2. Brazilian National Council for Scientific and Technological Development (CNPq) [307669/2019-0]

向作者/读者索取更多资源

This study evaluated the effects of a physical exercise program on animals with experimental glioblastoma. The results showed that the trained animals exhibited changes in behavior and lower expression of certain proteins related to tumorigenesis. However, no significant alterations were observed in oxidative stress and inflammatory mediators after physical exercise. These findings provide consistent evidence for the relationship between exercise and improvement in tumorigenic parameters against neurotoxicity.
Glioma 261 (Gl261) cell-mediated neurotoxicity has been reported in previous studies examining glioblastoma (GBM), and the effects of physical exercise (PE) on this neurotoxicity have been poorly investigated. This study aimed to evaluate the effects of a PE program in animals with experimental GBM. Male C57BL/6J mice were randomized into sham or GBM groups and subjected to a PE program for four weeks. Gl261 cells were administered into the intraventricular region at 48 h after the last exercise session. Body weight, water and feed consumption, and behavior were all evaluated for 21 days followed by euthanasia. The right parietal lobe was removed for the analysis of glial fibrillary acidic protein (GFAP), epidermal growth factor receptor (EGFR), vimentin, C-myc, nuclear factor kappa B (NF-kappa B), tumor necrosis factor-alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), hydrogen peroxide, the glutathione system, and oxidative damage to proteins. The results revealed changes in the behavioral patterns of the trained animals, and no anatomopathological changes were observed in response to PE training. In contrast, animals with GBM subjected to PE exhibited lower immunoexpression of c-MYC, vimentin, and GFAP. Although experimental GBM altered the redox profile and inflammatory mediators, no significant alterations were observed after PE. In conclusion, our data provide consistent evidence of the relationship between PE and the improvement of tumorigenic parameters against the neurotoxicity of GL261 cells.

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