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Updated: Feb 10, 2026
06:01
A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
15.6K
The isothiocyanate sulforaphane modulates platelet function and protects against cerebral thrombotic dysfunction
Scarlett Gillespie1, Paul M Holloway1,2, Felix Becker3
1Division of Brain Sciences, Imperial College London, London, UK.
British Journal of Pharmacology
|May 26, 2018
Summary
Sulforaphane (SFN) reduces inflammation-enhanced blood clot formation in the brain. This natural compound also improves platelet function, offering potential protection against stroke in high-risk individuals.
Area of Science:
- Biochemistry
- Pharmacology
- Neuroscience
Background:
- Platelet activation links inflammation and thrombosis.
- Sulforaphane (SFN) exhibits anti-inflammatory and anti-thrombotic effects.
- Inflammation and thrombosis are interconnected processes.
Purpose of the Study:
- Investigate SFN's effect on inflammation-potentiated thrombosis.
- Assess SFN's impact on platelet activation and thrombus formation in the brain's microvasculature.
Main Methods:
- Induced thrombosis in murine brains using light/dye-injury model with LPS.
- Administered SFN with and without LPS.
- Conducted in vitro and in vivo platelet function assays (aggregation, adhesion, calcium signaling) using human and murine platelets.
Main Results:
- SFN reduced LPS-enhanced thrombus formation in the cerebral microcirculation.
- SFN protected against LPS-induced prolonged bleeding time by improving platelet function.
- SFN inhibited collagen-mediated platelet aggregation, adhesion, and calcium signaling, involving glycoprotein VI.
Conclusions:
- SFN mitigates inflammatory potentiation of cerebral thrombosis.
- SFN normalizes LPS-impaired platelet function.
- SFN shows promise for stroke prevention in high-risk patients.
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