UPLC-Q-TOF/MS-based urine and plasma metabonomics study on the ameliorative effects of aspirin eugenol ester in hyperlipidemia rats

Ma, Ning; Karam, Isam; Liu, Xi-Wang; Kong, Xiaojun; Qin, Zhe; Li, Shihong; Jiao, Zeng-Hua; Dong, Ping; Yang, Yajun; Li, Jianyong

doi:10.1016/j.taap.2017.07.013

Cited by 43 publications

(28 citation statements)

References 54 publications

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“…Regulation effects of AEE on blood lipids in hyperlipidemic rats has been confirmed in our previous study, in which 54 mg/kg AEE significantly reduced TG, TCH, LDL, and elevated HDL [ 10 ]. Our previous plasma and urine metabonomic study has revealed that the effects of AEE against hyperlipidemia may involve in regulating the perturbation of glycerophospholipid metabolism, fatty acid metabolism, fatty acid beta-oxidation, amino acid metabolism, TCA cycle, sphingolipid metabolism, pyrimidine metabolism and gut microflora [ 11 ]. Meanwhile, feces and liver tissue, as important biological samples, may be attractive for biomarker investigation to provide a new insight into the progression of hyperlipidemia and the therapeutic basis of AEE.…”

Section: Introductionmentioning

confidence: 99%

Feces and liver tissue metabonomics studies on the regulatory effect of aspirin eugenol eater in hyperlipidemic rats

Liu

Kong

et al. 2017

Lipids Health Dis

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BackgroundBased on the pro-drug principle, aspirin and eugenol were esterified to synthesize aspirin eugenol ester (AEE). The anti-hyperlipidemia effect of aspirin eugenol ester has been confirmed in hyperlipidemic rat induced by high fat diet (HFD). However, its effect on liver and feces metabonomic profiles remains unknown.MethodsSuspension of AEE was prepared in 5% carboxymethyl cellulose sodium (CMC-Na). Thirty rats were divided into control, model and AEE groups. The control and model rats were fed with normal diet or HFD for 13 weeks, respectively. Rats in AEE-treated group were fed with HFD for 8 weeks to induce hyperlipidemia, and then given AEE once daily by oral gavage for 5 weeks at the dosage of 54 mg/kg body weight. After drug intervention, lipid profile analysis and oil red O staining were carried out to confirm the lipid accumulation in liver tissue. UPLC-Q-TOF/MS-based liver and feces metabonomics coupled with pathway analysis were conducted to evaluate the changes of metabolic profile and endogenous metabolites.ResultsIn liver tissue, oral administration of AEE significantly reduced lipid droplets and the levels of triglyceride (TG) and low-density lipoprotein (LDL). Using principal component analysis (PCA) and partial least squares-discriminate analysis (PLS-DA), distinct changes in metabolite patterns in feces and liver were observed. Liver and feces samples in control, model and AEE groups were scattered in PLS-DA score plots. 28 metabolites in liver and 22 in feces were identified as potential biomarkers related to hyperlipidemia. As possible drug targets, the perturbations of those biomarkers can be regulated by administration of AEE.ConclusionAnti-hyperlipidemia effect of AEE was confirmed by lipid analysis, oil red O staining and metabolomics analysis. The mechanism of AEE might be associated with the changes in the metabolism of glycerophospholipid, amino acid, fatty acid, sphingolipid, purine, bile acid and glutathione.Electronic supplementary materialThe online version of this article (10.1186/s12944-017-0633-0) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Feces and liver tissue metabonomics studies on the regulatory effect of aspirin eugenol eater in hyperlipidemic rats

Liu

Kong

et al. 2017

Lipids Health Dis

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“…Alterations in lipids metabolism are associated and suggested as causative for the pathophysiology of in ammation-related diseases such as atherosclerosis, diabetes, cancer and dyslipidemia [35,36] . In addition, previous studies have also shown that they are associated with the mechanism of ulcer induced by ethanol [37] .…”

Section: Discussionmentioning

confidence: 99%

Study on the Protective Effect and the Metabolomics Features of Rutaecarpine on Ethanol-induced Acute Gastric Ulcer

Ren

Wei

Niu

et al. 2020

Preprint

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As a prevalent digestive disease, Gastric ulcer (GU) has a high incidence and is seriously harmful to human health. It is an urgent need to finding a natural drug with a gastroprotective effect. Rutaecarpine (RUT) is an alkaloid isolated from Evodia rutaecarpa Bentham (Rutaceae). This plant is a traditional Chinese medicine that has been treating gastrointestinal diseases for a long time. The present study aimed to investigate the effects of RUT on ethanol-induced acute GU in mice. After intragastrical administration of RUT for 3 consecutive days, acute GU were induced in the mice by ethanol treatment for 1.5 h. The expression levels of SOD, CAT, NO, ET-1 in serum and EGF, TNF-α, IL-1β, IL-6 in gastric tissues were measured by kits. In addition, hematoxylin and eosin (H&E) staining of gastric mucosa for pathological changes was evaluated. The serum metabolomics method based on ultra-high-performance liquid chromatography combined with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) was used to explore the potential mechanism. A total of 7 potential metabolites involved in 9 metabolic pathways were identified. This study helps us to further understand the pathogenesis of GU and provide a potential natural anti-ulcer drug for clinic.

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“…With few exceptions [47,48], the effect of ASA on the increase of mitochondrial fatty acid oxidation has been documented in different cell lines, and interpreted as a compensatory shift from carbohydrate metabolism to FA oxidation [46]. Involvement of the β-oxidation pathway in the effect of a pro-drug formulation of ASA has also been reported in an animal model of hyperlipidemia [49]. occurrence of the expected ASA metabolites-i.e., salicylic acid, salicyluric acid, and 5-sulfosalicylic acid-in the samples collected after treatment.…”

Section: Discussionmentioning

confidence: 99%

Untargeted Metabolomics to Go beyond the Canonical Effect of Acetylsalicylic Acid

Minno

Porro

Turnu

et al. 2019

JCM

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Given to its ability to irreversibly acetylate the platelet cyclooxygenase-1 enzyme, acetylsalicylic acid (ASA) is successfully employed for the prevention of cardiovascular disease. Recently, an antitumoral effect of ASA in colorectal cancer has been increasingly documented. However, the molecular and metabolic mechanisms by which ASA exerts such effect is largely unknown. Using a new, untargeted liquid chromatography–mass spectrometry approach, we have analyzed urine samples from seven healthy participants that each ingested 100 mg of ASA once daily for 1 week. Of the 2007 features detected, 25 metabolites differing after ASA ingestion (nominal p < 0.05 and variable importance in projection (VIP) score > 1) were identified, and pathway analysis revealed low levels of glutamine and of metabolites involved in histidine and purine metabolisms. Likewise, consistent with an altered fatty acid β-oxidation process, a decrease in several short- and medium-chain acyl-carnitines was observed. An abnormal β-oxidation and a lower than normal glutamine availability suggests reduced synthesis of acetyl-Co-A, as they are events linked to one another and experimentally related to ASA antiproliferative effects. While giving an example of how untargeted metabolomics allows us to explore new clinical applications of drugs, the present data provide a direction to be pursued to test the therapeutic effects of ASA—e.g., the antitumoral effect—beyond cardiovascular protection.

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UPLC-Q-TOF/MS-based urine and plasma metabonomics study on the ameliorative effects of aspirin eugenol ester in hyperlipidemia rats

Cited by 43 publications

References 54 publications

Feces and liver tissue metabonomics studies on the regulatory effect of aspirin eugenol eater in hyperlipidemic rats

Feces and liver tissue metabonomics studies on the regulatory effect of aspirin eugenol eater in hyperlipidemic rats

Study on the Protective Effect and the Metabolomics Features of Rutaecarpine on Ethanol-induced Acute Gastric Ulcer

Untargeted Metabolomics to Go beyond the Canonical Effect of Acetylsalicylic Acid

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