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

Neurochem Res. 2022 Nov;47(11):3344-3354. doi: 10.1007/s11064-022-03685-y. Epub 2022 Jul 29.

Abstract

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-κB), tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), 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.

Keywords: Brain tumor; Glioblastoma; Inflammation; Oxidative stress; Physical exercise.

Publication types

  • Randomized Controlled Trial, Veterinary

MeSH terms

  • Animals
  • Brain / metabolism
  • ErbB Receptors / metabolism
  • Glial Fibrillary Acidic Protein / metabolism
  • Glioblastoma* / pathology
  • Glioma* / pathology
  • Glutathione
  • Hydrogen Peroxide
  • Inflammation Mediators / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Models, Theoretical
  • NF-kappa B / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Vimentin / metabolism
  • Water

Substances

  • Glial Fibrillary Acidic Protein
  • Inflammation Mediators
  • Interleukin-1beta
  • Interleukin-6
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Vimentin
  • Water
  • Hydrogen Peroxide
  • ErbB Receptors
  • Glutathione