UPLC-Q-TOF/MS-Based Plasma Metabolomics to Evaluate the Effects of Aspirin Eugenol Ester on Blood Stasis in Rats

Aspirin eugenol ester (AEE) is a novel compound that is formed from the esterification of aspirin (acetylsalicylic acid (ASA)) and eugenol. This study aimed to investigate the effects of AEE on blood stasis in rats and to characterize the underlying mechanisms using a plasma metabolomic study. The r...

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Bibliographic Details
Main Authors: Dongshuai Shen, Ning Ma, Yajun Yang, Xiwang Liu, Zhe Qin, Shihong Li, Zenghua Jiao, Xiaojun Kong, Jianyong Li
Format: Article
Language:English
Published: MDPI AG 2019-06-01
Series:Molecules
Subjects:
Online Access:https://www.mdpi.com/1420-3049/24/13/2380
Description
Summary:Aspirin eugenol ester (AEE) is a novel compound that is formed from the esterification of aspirin (acetylsalicylic acid (ASA)) and eugenol. This study aimed to investigate the effects of AEE on blood stasis in rats and to characterize the underlying mechanisms using a plasma metabolomic study. The results indicate that AEE and ASA could modulate whole blood viscosity (WBV), plasma viscosity (PV), blood coagulation parameters, platelet count, platelet aggregation, lactate dehydrogenase (LDH), creatinine (CR) and the levels of thromboxane A2 (TXA<sub>2</sub>) and 6-keto prostaglandin F1&#945; (6-keto-PGF<sub>1&#945;</sub>). The metabolic profiles of the plasma samples from all groups were clearly separated in the score plots. Nineteen potential metabolites were selected and identified, and disordered levels of these metabolites could be regulated by AEE and ASA. Pathway analysis showed that the mechanism of action of AEE on blood stasis might be principally related to the metabolism of amino acid, fatty acid, energy and glycerophospholipid. The above results indicate that AEE protected the rats against blood stasis, and that this effect might have been caused by the anticoagulation activity of AEE and its abilities to maintain a balance between TXA<sub>2</sub> and PGI<sub>2</sub>, reduce blood viscosity, inhibit platelet aggregation and normalize the plasma metabolic profile.
ISSN:1420-3049