Reduction of microglial activity in a model of multiple sclerosis by dipyridamole
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BACKGROUND: Despite extensive and persistent activation of microglia in multiple sclerosis (MS), microglia inhibitors have not yet been identified for treatment of the disorder. We sought to identify medications already in clinical use that could inhibit the activation of microglia. On the basis of the reported inhibitory effects of dipyridamole on phosphodiesterase activity that result in the production of various anti-inflammatory outcomes, we selected it for study. Dipyridamole is used clinically for secondary prevention in stroke. In this study, dipyridamole was examined using microglia in culture and in the mouse model of MS, experimental autoimmune encephalomyelitis (EAE). RESULTS: We found that dipyridamole attenuated the elevation of several cytokines and chemokines in human microglia caused by Toll-like receptor stimulation. Morphological characteristics of activated microglia in culture were also normalized by dipyridamole. In mice, dipyridamole decreased the clinical severity of EAE and reduced microglial activity and other histological indices of EAE in the spinal cord. CONCLUSIONS: Dipyridamole is an inhibitor of microglia activation and may have a role in MS and other neurological conditions to attenuate microglial activity.
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Dipyridamole attenuates expression of Toll-like receptor stimulation-dependent cytokines and chemokines in human microglia, reduces microglial activity in EAE mice, and consequently decreases IL-1β, TNF-α and IL-6 expression, which are responsible for increased BBB permeability.
“Recently published data demonstrated that dipyridamole attenuates the expression of Toll-like receptor stimulation-dependent cytokines and chemokines in human microglia, reduces microglial activity in EAE mice, and consequently decreases IL-1β, TNF-α and IL-6 expression, which are responsible for increased BBB permeability (Sloka et al., 2013).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Sloka et al., 2013
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- Authors
- Sloka, S., Metz, L. M., Hader, W., Starreveld, Y., & Yong, V. W.
- Affiliations
- University of Calgary (CA)
- Corresponding author
- Yong, V Wee
- Venue
- Journal of Neuroinflammation
- Published
- 2013-07-18
- Volume
- 10
- Issue
- 1
- Pages
- 89-89
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3724584
- OpenAlex
- W2080652296
- Cited by
- 53
- References
- 52
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 7 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 9
- FWCI
- 3.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Heart and Stroke Foundation of Canada
- Biogen
- Multiple Sclerosis Society of Canada
- Multiple Sclerosis Society
- Fondation pour la Recherche Médicale
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- dipyridamole, microglial activation, multiple sclerosis, experimental autoimmune encephalomyelitis, phosphodiesterase inhibition, Toll-like receptor activation, cytokines, chemokines, microglial morphology, neuroinflammation, anti-inflammatory therapy
- MeSH terms
- Adenosine Triphosphate, Animals, Cell Survival, Cells, Cultured, Dipyridamole, Encephalomyelitis, Autoimmune, Experimental, Female, Fluorescent Antibody Technique, Humans, Image Processing, Computer-Assisted, Lipopolysaccharides, Macrophages, Mice, Inbred C57BL, Multiple Sclerosis, Phagocytosis, Platelet Aggregation Inhibitors, Cytokines, Culture Media, Conditioned, Microglia, Mice, In Vitro Techniques
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