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Updated: May 25, 2026

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
Published on: January 18, 2017
Paradoxical effect of aspirin.
Christian Doutremepuich1, Omar Aguejouf, Vanessa Desplat
1Laboratoire d'Hématologie, Université Bordeaux Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France.
Low-dose aspirin is safe for preventing heart attacks and strokes, with benefits outweighing bleeding risks. High aspirin doses can cause hemorrhage, but low doses do not, especially in specific genetic contexts.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hemorrhagic Stroke Research
Background:
- Low-dose aspirin is a cost-effective option for secondary prevention of myocardial infarction (MI) and ischemic stroke.
- Aspirin is also used in primary MI prevention, but its risks, particularly hemorrhagic stroke, require careful consideration.
- Balancing aspirin's cardiovascular benefits against hemorrhage risks is crucial for clinical decision-making.
Purpose of the Study:
- To clarify the risks of aspirin use concerning hemorrhagic stroke.
- To investigate the dose-dependent effects of aspirin on hemorrhage.
- To explore the role of cyclooxygenase (COX) enzymes in aspirin-induced bleeding.
Main Methods:
- Normal, COX-1 knockout, and COX-2 knockout mice were used.
- Mice were treated with a wide range of aspirin doses.
- Induced hemorrhagic time was measured to assess bleeding risk.
Main Results:
- High doses of aspirin were found to induce hemorrhage.
- Low doses of aspirin did not significantly increase hemorrhage risk.
- In COX-1 knockout mice, ultra-low aspirin doses showed an anti-hemorrhagic effect, unlike intermediate doses.
- COX-2 deficiency led to a hemorrhagic effect requiring further investigation.
Conclusions:
- Aspirin's effect on hemorrhage is dose-dependent; low doses are generally safe.
- Cyclooxygenase pathways play a critical role in aspirin's impact on bleeding.
- Further research is needed to understand the hemorrhagic effects observed in COX-2 deficient mice.
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