Cited by 37Stress Responses and CortisolExercise and Physiological ResponsesNeuroinflammation and Neurodegeneration Mechanisms

Exercise protects against chronic restraint stress-induced oxidative stress in the cortex and hippocampus

Gerecke, Kim M., Kolobova, Anna, Allen, Sarah, Fawer, Jessica L.·2013·Brain Research

Abstract

Chronic stress induces high levels of reactive oxygen species, creating a neurotoxic environment. Because exercise protects against the neurodegenerative effects of oxidative stress, we investigated the protective effects of exercise against chronic restraint stress (CRS)-induced expression of the proapoptotic cortical B-cell associated X protein (Bax) and cyclooxegenase-2 (Cox-2) as well as microglial/macrophage proliferation and co-expression of Cox-2 in the cortex and hippocampus of mice. CRS induced a large, moderately significant increase in protein levels of Bax 1 h following stress. However, exercised mice had significantly lower cortical levels of Bax at both the 1 and 24 h time points. The level of Cox-2 protein was also significantly lower in the cortex of exercised mice. While no significant changes in microglia/macrophage proliferation were observed in either brain region, CRS induced significant increases of Cox-2 labeling on microglia/macrophages in both the hippocampus and cortex of stressed mice. In the cortex, stressed mice showed significantly greater numbers of Iba1/Cox-2 co-labeled cells than non-stressed mice; however, exercise alone did not induce any changes. In the hippocampus, CRS induced significantly greater numbers of Cox-2 labeled microglia/macrophages in stressed sedentary animals as compared to non-stressed controls. However, exercised mice were protected against these increases, as there was no significant difference in the numbers of Iba1/Cox-2 co-labeled cells between stressed and non-stressed exercised mice. Therefore, exercise protects against CRS-induced increases in levels of Bax in the cortex, and microglial/macrophage expression of Cox-2 in the hippocampus. Taken together, these data suggest that exercise may confer neuroprotection by acting to increase the resilience of the brain against CRS-induced oxidative stress.

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Crossref · 10.1016/j.brainres.2013.02.027

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Authors
Gerecke, K. M., Kolobova, A., Allen, S., & Fawer, J. L.
Affiliations
Rhodes College (US)
Corresponding author
Gerecke, Kim M.
Venue
Brain Research
Publisher
Elsevier BV
Published
2013-05
Volume
1509
Pages
66-78
ISSN
0006-8993 (ISSN-L)
OpenAlex
W2040796363
Cited by
37
References
135
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 3 · 2014: 10 · 2013: 1
FWCI
2.40
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
Rhodes College
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
physical activity, chronic restraint stress, oxidative stress, neuroprotection, Bax, cyclooxygenase-2, microglia, macrophages, hippocampus, cortex, reactive oxygen species, neurodegeneration, stress resilience
MeSH terms
Animals, Cerebral Cortex, Female, Hippocampus, Nerve Degeneration, Physical Conditioning, Animal, Restraint, Physical, Stress, Physiological, Stress, Psychological, Microglia, Oxidative Stress, bcl-2-Associated X Protein, Mice, Cyclooxygenase 2

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