Cyclooxygenase-1 Mediated Platelet Reactivity in Young Male Smokers

Loke, Wai Mun; Sing, Karen Lam Mok; Lee, Jetty Chung‐Yung; Chong, Wan Ling; Chew, Soh Eng; Huang, Hui-Wen; Looi, Woan Foon; Quek, Amy M.L.; Lim, Erle C.H.; Seet, Raymond C.S.

doi:10.1177/1076029612466284

Cited by 13 publications

(8 citation statements)

References 27 publications

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“…A chromogenic procedure stablished on the oxidation of N , N , N ′, N ′-tetramethyl-p- phenylenediamine (TMPD) while the PGG 2 reduced to PGH 2 , determined the COX-1 activity [ 46 ]. AA was transformed into PGG 2 in the platelet aggregation pathway, and this prostacyclin was immediately reduced to PGH 2 by COX-1, thus, TMPD was proportionally oxidized to the enzyme activity.…”

Section: Methodsmentioning

confidence: 99%

Flavonoids: Antiplatelet Effect as Inhibitors of COX-1

et al. 2022

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Flavonoids are compounds with a benzopyranic structure that exhibits multiple pharmacological activities. They are known for their venotonic activity, but their mechanism of action remains unclear. It is thought that, as this mechanism is mediated by prostaglandins, these compounds may interfere with the arachidonic acid (AA) cascade. These assays are designed to measure the antiplatelet aggregation capacity of quercetin, rutin, diosmetin, diosmin, and hidrosmin, as well as to evaluate a potential structure−activity ratio. In this paper, several studies on platelet aggregation at different concentrations (from 0.33 mM to 1.5 mM) of different flavone compounds are conducted, measuring platelet aggregation by impedance aggregometry, and the cyclooxygenase (COX) activity by metabolites generated, including the activity of the pure recombinant enzyme in the presence of these polyphenols. The results obtained showed that quercetin and diosmetin aglycones have a greater antiplatelet effect and inhibit the COX enzyme activity to a greater extent than their heterosides; however, the fact that greater inhibition of the pure recombinant enzyme was achieved by heterosides suggests that these compounds may have difficulty in crossing biological membranes. In any case, in view of the results obtained, it can be concluded that flavonoids could be useful as coadjuvants in the treatment of cardiovascular pathologies.

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Section: Methodsmentioning

confidence: 99%

Flavonoids: Antiplatelet Effect as Inhibitors of COX-1

et al. 2022

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“…Of the 21 studies, ten were included in the meta-analyses [ 10 , 14 , [18] , [19] , [20] , [21] , [22] , [23] , [24] , [25] ]. The other 11 studies were not included due to having incomplete information [ 26 , 27 ], results given in different units [ [28] , [29] , [30] , [31] ], study results had been published in another study [ 1 , 32 ], measurements were reported from plasma concentrations [ 13 ] or included diseased populations [ 33 , 34 ]. Characteristics of all studies included in the analyses can be found in Table 1 .…”

Section: Resultsmentioning

confidence: 99%

Influence of smoking and smoking cessation on levels of urinary 11-dehydro thromboxane B2

et al. 2018

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BackgroundThromboxane is a key clinical risk endpoint of smoking-induced inflammation which has been associated in the pathogenesis of cardiovascular disease. The goal of this review is to quantify the effect of smoking and smoking cessation on one of its urinary metabolites, 11-dehydrothromboxaneB2.MethodsPubMed and SCOPUS were searched to identify publications which report urinary 11-dehydrothromboxaneB2 levels in smokers and non-smokers, as well as articles reporting the effect of smoking cessation on urinary 11-dehydrothromboxaneB2 excretion.ResultsWe found ten studies assessing urinary 11-dehydrothroboxaneB2 levels in smokers and non-smokers. Four papers reported the amount of urinary 11-dehydrothromboxaneB2 excreted in 24 h while six reported the amount excreted adjusted for creatinine. The meta-analyses comparing the excretion of urinary 11-dehydrothromboxane in current smokers to non-smokers report increased levels in current smokers (mean difference = 0.31 μg/24-h [95%CI: 0.27–0.34] and 166.45 pg/mg creatinine [95%CI: 120.51–212.40]). There were not enough publications to perform meta-analyses on the effects of smoking cessation on urinary 11-dehydrothromboxaneB2 excretion.ConclusionsUrinary 11-dehydrothromboxaneB2 levels are increased in cigarette smokers, however, more data are needed to elucidate the effects of smoking cessation on urinary 11-dehydrothromboxaneB2 excretion.

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“…Increased platelet reactivity promotes dysregulated platelet aggregation which is associated with increased risk of myocardial infarction, terminal occlusive thrombotic events, and sudden death in patients with COPD (Brassington et al, 2019). Firstly, CS exposure has been shown to directly cause platelet activation and their aggregation via the activation of the Cyclooxygenase-1 pathway (Loke et al, 2014). Secondly, the spillover of pro-inflammatory mediators from the COPD lungs into the vasculature may causes the adhesion of activated platelets to the arterial wall and collagen fibres, via the up-regulation of CD41, p-selectin (CD62p) and von Willibrand factor (Jennings, 2009).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of oxidative stress by apocynin attenuated COPD progression and vascular injury by cigarette smoke exposure

Chan

Brassington

Almerdasi

et al. 2022

Preprint

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Background and Purpose: Cardiovascular disease (CVD) affects up to half of the patients with chronic obstructive pulmonary disease (COPD), which exerts deleterious impact on health outcomes and survivability. Vascular endothelial dysfunction marks the onset of cardiovascular disease. The present study examined the effect of a potent NADPH Oxidase (NOX) inhibitor and free-radical scavenger, apocynin, on COPD-related CVD. Experimental Approach: Male BALB/c mice were exposed to either room air (Sham) or cigarette smoke (CS) generated from 9 cigarettes per day, 5 days a week for up to 24 weeks with or without apocynin treatment (5 mg·kg-1·day-1, intraperitoneal injection). Key Results: Eight-weeks of apocynin treatment reduced airway neutrophil infiltration (by 42%) and completely preserved endothelial function and endothelial nitric oxide synthase (eNOS) activity against the oxidative insults of CS exposure. These preservative effects were maintained up until the 24-week time point. 24-week of apocynin treatment exhibited marked benefits on airway inflammation (reduced infiltration of macrophage, neutrophil and lymphocyte) and lung function decline (hyperinflation), and prevented airway collagen deposition by CS exposure. Conclusion and Implications: Limiting NOX activity may slow COPD progression and lower CVD risk, particularly when signs of oxidative stress become evident.

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Cyclooxygenase-1 Mediated Platelet Reactivity in Young Male Smokers

Abstract: Cigarette smoking aggravates COX-1-mediated platelet reactivity in young, otherwise healthy, smoking men.

Cited by 13 publications

References 27 publications

Flavonoids: Antiplatelet Effect as Inhibitors of COX-1

Flavonoids: Antiplatelet Effect as Inhibitors of COX-1

Influence of smoking and smoking cessation on levels of urinary 11-dehydro thromboxane B2

Inhibition of oxidative stress by apocynin attenuated COPD progression and vascular injury by cigarette smoke exposure

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