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Published on: June 29, 2015
Protective effects of triflusal on secondary thrombus growth and vascular cyclooxygenase-2
X Duran1, S Sánchez, G Vilahur
1Cardiovascular Research Center, CSIC-ICCC, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Insights
Aspirin, triflusal, and HTB effectively reduced secondary thrombus growth. Triflusal better preserved Cox-2 expression, while HTB maintained endothelial prostacyclin production, offering distinct benefits in preventing cerebrovascular ischemia.
Area of Science:
- Pharmacology and Thrombosis Research
- Vascular Biology and Inflammation
- Cardiovascular Disease Prevention
Background:
- Carotid residual mural thrombus is a significant risk factor for recurrent thrombosis and embolization, leading to cerebrovascular ischemia.
- Understanding the mechanisms of thrombus formation and the efficacy of antiplatelet agents is crucial for preventing ischemic events.
Purpose of the Study:
- To compare the efficacy of aspirin, triflusal, and its metabolite HTB in inhibiting secondary thrombus growth.
- To evaluate the impact of these cyclooxygenase-1 (Cox-1) inhibitors on vascular Cox-1/Cox-2 expression and endothelial prostacyclin synthesis.
Main Methods:
- A rabbit model of ex vivo carotid thrombosis was used to assess secondary thrombus growth after intravenous and oral administration of aspirin, triflusal, and HTB.
- Secondary thrombus formation was quantified using In-(111)-deposited platelets.
- Vascular Cox-1/Cox-2 expression (mRNA and protein) and endothelial prostacyclin (PGI2) release were measured.
Main Results:
- All tested Cox-1 inhibitors significantly reduced secondary thrombus formation compared to placebo.
- Aspirin and triflusal moderately reduced vascular Cox-2 mRNA expression, with triflusal showing slightly higher Cox-2 protein levels than aspirin.
- In vitro, 2-hydroxy-4-trifluorometylbenzoic acid (HTB) uniquely maintained endothelial prostacyclin synthesis.
Conclusions:
- Triflusal and aspirin demonstrate comparable efficacy in inhibiting secondary thrombosis.
- Triflusal appears to preserve vascular Cox-2 expression more effectively than aspirin.
- HTB plays a role in protecting endothelial prostacyclin production, suggesting a multifaceted therapeutic potential.
Background:
Carotid residual mural thrombus predisposes to recurrent thrombosis and/or distal embolization (i.e. cerebrovascular ischemia).
Objectives:
Our aims were (i) to analyze and compare the efficacy of aspirin, triflusal, and its main metabolite 2-hydroxy-4-trifluorometylbenzoic acid (HTB) on secondary thrombus growth; and (ii) evaluate to what extent the three Cox-1 inhibitors influenced vascular Cox-1/Cox-2 expression and endothelial prostacyclin synthesis.
Methods:
In a rabbit model of ex vivo thrombosis, a fresh mural thrombus was formed on damaged vessels at flow conditions typical of mild and severe carotid stenoses. The effects of Cox-1 inhibitors administered both intravenously (i.v.) (aspirin 5 mg kg(-1), triflusal 10 mg kg(-1), and HTB 10 mg kg(-1)) and orally (p.o.) (8 days; aspirin 30 mg kg(-1) day(-1), and triflusal 40 mg kg(-1) day(-1)) on secondary thrombus growth were assessed by In-(111)deposited platelets and compared with a placebo control. Arterial Cox-1/Cox-2 expression after 8-day treatment was evaluated at mRNA and protein levels. Additionally, a drug-related dose-dependent in vitro assay was performed for endothelial PGI(2) release measurement (Cox-2 activity).
Results:
All Cox inhibitors similarly and significantly (P < 0.05) reduced secondary thrombus formation after i.v. and p.o. administration versus placebo control. Treatments exerted no effect on vascular Cox-1 mRNA whereas Cox-2 mRNA was moderately reduced by aspirin and triflusal (placebo 100% +/- 9%, aspirin 70% +/- 2% and triflusal 70% +/- 2%; P < 0.05). Cox-2 protein levels were slightly higher in the triflusal versus aspirin group (placebo 100% +/- 6%, aspirin 35% +/- 10% and triflusal 61% +/- 9%; P < 0.005 versus placebo). Interestingly, in vitro, HTB solely maintained endothelial PGI(2) synthesis levels similar to the control.
Conclusions:
At a similar level of efficacy in inhibiting secondary thrombosis, triflusal seems to better preserve Cox-2 expression than aspirin and its metabolite HTB was able to protect endothelial prostacyclin production.
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