Key result
Aspirin eugenol ester significantly inhibited arachidonic acid-induced platelet aggregation and reduced blood viscosity more effectively than its precursors in a rat thrombosis model.
Why the study?
Does aspirin eugenol ester improve antithrombotic effects compared to its precursors in a rat model of thrombosis?
Does aspirin eugenol ester improve antithrombotic effects compared to its precursors in a rat model of thrombosis?
Aspirin eugenol ester demonstrates superior antithrombotic and antiplatelet effects compared to its precursors in a rat model, suggesting potential as a novel therapeutic agent.
Answers are grounded in this paper and cite their sources.
AEE showed antithrombotic activity in a rat model; leaves open translation to clinical veterinary use.
BACKGROUND: Based on the prodrug principle, aspirin and eugenol, as starting precursors, were esterified to synthesize aspirin eugenol ester (AEE). The aim of the present study was to evaluate the antithrombotic effect of AEE in an animal disease model. In order to compare the therapeutic effects of AEE and its precursors, aspirin, eugenol and a combination of aspirin and eugenol were designed at the same molar quantities as the AEE medium dose in the control group. METHODS: After oral administration of AEE (dosed at 18, 36 and 72 mg/kg) for seven days, rats were treated with k-carrageenan to induce tail thrombosis. Following the same method, aspirin (20 mg/kg), eugenol (18 mg/kg) and 0.5 % CMC-Na (30 mg/kg) were administered as control drug. Different drug effects on platelet aggregation, hemorheology, TXB2/6-keto-PGF1α ratio and blood biochemistry were studied. RESULTS: AEE significantly inhibited ADP and AA-induced platelet aggregation in vivo. AEE also significantly reduced blood and plasma viscosity. Moreover, AEE down-regulated TXB2 and up-regulated 6-keto-PGF1α, normalizing the TXB2/6-keto-PGF1α ratio and blood biochemical profile. In comparison with aspirin and eugenol, AEE produced more positive therapeutic effects than its precursors under the same molar quantity. CONCLUSION: It may be concluded that AEE was a good candidate for new antithrombotic and antiplatelet medicine. Additionally, this study may help to understand how AEE works on antithrombosis in different ways.
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Ma et al. (2016) studied k-carrageenan-induced tail thrombosis (n=90). Aspirin eugenol ester (AEE) vs. 0.5% CMC-Na (vehicle), aspirin, eugenol, and combination was evaluated on AA-induced platelet aggregation (%) (p=<0.01). Aspirin eugenol ester significantly inhibited arachidonic acid-induced platelet aggregation and reduced blood viscosity more effectively than its precursors in a rat thrombosis model.
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