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Cited by 45Acute Ischemic Stroke ManagementNeuroinflammation and Neurodegeneration MechanismsNeurological Disorders and Treatments

The role of tumor necrosis factor-alpha in stress-induced worsening of cerebral ischemia in rats

Caso, J.R., Lizasoain, I., Lorenzo, P., Moro, M.A., Leza, J.C.·2006·Neuroscience
DOI 10.1016/j.neuroscience.2006.06.009
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Abstract

Whereas stress is known to be one of the risk factors of stroke, few experimental studies have examined the possible mechanisms by which stress may affect stroke outcome. Most of the knowledge on the effects of stress on cerebrovascular disease in humans is restricted to catecholamines and glucocorticoids effects on blood pressure and/or development of atherosclerosis. By using an experimental paradigm consisting of the exposure of Fischer rats to repeated immobilization sessions (1 h daily during seven consecutive days) prior to permanent middle cerebral artery occlusion (MCAO), we have found that stress worsens behavioral outcome and increases infarct size after MCAO. These changes occur concomitantly to an increase in inducible nitric oxide synthase (iNOS) expression and to the accumulation of lipid peroxidation markers in brain tissue. The possible regulatory role of TNFalpha was studied by looking at the mechanisms of release of this cytokine as well as to the expression of its receptors (TNFR1 and 2). The results of the present study suggest an increase in TNFalpha expression and release after stress, as well as an increase in the expression of TNFR1. Pharmacological blockade of TNFalpha with anti-TNFalpha led to a decrease in the infarct size as well as in the oxidative/nitrosative biochemical parameters seen after ischemia. In summary, our results indicate that TNFalpha accounts, at least partly, for the worsening of MCAO consequences in brain of rats exposed to stress. Furthermore, the data presented here provide evidence that stress can increase brain ischemic damage and support a possible protective effect of treatment of stressful situations before and during the development of the brain ischemia.

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  • Subacute stress induces an increase in TNF-α levels in the cortex, and blocking this increase lessens stroke damage.

    “Moreover, subacute stress induces an increase in TNF-α levels in the cortex, and blocking this increase lessens stroke damage (Caso et al., 2006).”

    From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Caso et al., 2006

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Authors
Caso, J. R., Lizasoain, I., Lorenzo, P., Moro, M. A., & Leza, J. C.
Affiliations
Universidad Complutense de Madrid (ES)
Corresponding author
Leza, J.C.
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
2006-09
Volume
142
Issue
1
Pages
59-69
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2006.06.009
OpenAlex
W2078587552
Cited by
45
References
69
Citations by year
2022: 3 · 2021: 4 · 2019: 1 · 2018: 2 · 2017: 1 · 2015: 1 · 2014: 4 · 2013: 2 · 2012: 2
FWCI
3.65
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
TNF-α, psychological stress, cerebral ischemia, middle cerebral artery occlusion, infarct size, inducible nitric oxide synthase, lipid peroxidation, oxidative stress, nitrosative stress, TNF receptor 1, anti-TNF therapy, restraint stress, stroke risk factors
MeSH terms
ADAM17 Protein, Animals, Antibodies, Behavior, Animal, Brain Ischemia, Corticosterone, Disease Models, Animal, Male, Rats, Inbred F344, Stress, Physiological, Tumor Necrosis Factor-alpha, Blotting, Western, Lipid Peroxidation, Disease Progression, Brain Infarction, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Rats, ADAM Proteins, Nitric Oxide Synthase Type II

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