Tumor Necrosis Factor-α: A Mediator of Focal Ischemic Brain Injury
Abstract
BACKGROUND AND PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) is a pleiotropic cytokine that rapidly upregulates in the brain after injury. The present study was designed to explore the pathophysiological significance of brain TNF-alpha in the ischemic brain by systematically evaluating the effects of lateral cerebroventricular administration of exogenous TNF-alpha and agents that block the effects of TNF-alpha on focal stroke and by examining the potential direct toxic effects of TNF-alpha on cultured neurons to better understand how TNF-alpha might mediate stroke injury. METHODS: TNF-alpha (2.5 or 25 pmol) was administered intracerebroventricularly to spontaneously hypertensive rats 24 hours before permanent or transient (80 minutes and 160 minutes) middle cerebral artery occlusion (MCAO). Animals were examined 24 hours later for neurological deficits and ischemic hemisphere necrosis and swelling. In some of these studies, neutralizing anti-TNF-alpha monoclonal antibody (mAb) (60 pmol) was injected intracerebroventricularly 30 minutes before exogenous TNF-alpha (25 pmol). In addition, the effects of blocking endogenous TNF-alpha on permanent focal ischemic injury were determined with the use of either mAb (60 pmol) or soluble TNF receptor I (sTNF-RI) (0.3 or 0.7 nmol) administered intracerebroventricularly 30 minutes before and 3 and 6 hours after MCAO. Finally, the direct neurotoxic effects of TNF-alpha were studied in cultured rat cerebellar granule cells exposed to TNF…
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TNFα signaling contributes to ischemic injury of neurons.
“TNFα signaling is well known to contribute to ischemic injury of neurons [23].”
From MicroRNA‐21 protects neurons from ischemic death (2010) · cites this paper as [23]
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References 83 · Cited by 863
- Authors
- Barone, F. C., Arvin, B., White, R. F., Miller, A., Webb, C. L., Willette, R. N., Lysko, P. G., & Feuerstein, G. Z.
- Affiliations
- Carmel Medical Center (IL)
- Venue
- Stroke
- Published
- 1997-06
- Volume
- 28
- Issue
- 6
- Pages
- 1233-1244
- ISSN
- 0039-2499 (ISSN-L)
- 1524-4628
- OpenAlex
- W2034882426
- Cited by
- 863
- References
- 83
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 19 · 2023: 11 · 2022: 14 · 2021: 28 · 2020: 16 · 2019: 13 · 2018: 16 · 2017: 16 · 2016: 39 · 2015: 36 · 2014: 45 · 2013: 32 · 2012: 34
- FWCI
- 28.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Stroke (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- TNF-α, ischemic stroke, middle cerebral artery occlusion, neuroinflammation, anti-TNF monoclonal antibody, soluble TNF receptor 1, cerebrovascular disease, glutamate excitotoxicity, neuronal cell death, infarct size, neurological deficit, cerebellar granule cells, spontaneously hypertensive rats
- MeSH terms
- Animals, Antibodies, Monoclonal, Cells, Cultured, Cerebellum, Cerebral Infarction, Brain Ischemia, Dose-Response Relationship, Drug, Male, Neurons, Rats, Inbred SHR, Tumor Necrosis Factor-alpha, Receptors, Tumor Necrosis Factor, Rats
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