Abstract
Catechol (benzenediol) is present in plant-derived products, such as vegetables, fruits, coffee, tea, wine, areca nut and cigarette smoke. Because platelet dysfunction is a risk factor of cardiovascular diseases, including stroke, atherosclerosis and myocardial infarction, the purpose of this study was to evaluate the anti-platelet and anti-inflammatory effect of catechol and its mechanisms. The effects of catechol on cyclooxygenase (COX) activity, arachidonic acid (AA)-induced aggregation, thromboxane B2 (TXB2) production, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production and extracellular signal-regulated kinase (ERK)/p38 phosphorylation were determined in rabbit platelets. In addition, its effect on IL-1β-induced prostaglandin E2 (PGE2) production by fibroblasts was determined. The ex vivo effect of catechol on platelet aggregation was also measured. Catechol (5-25 µM) suppressed AA-induced platelet aggregation and inhibited TXB2 production at concentrations of 0.5–5 µM; however, it showed little cytotoxicity and did not alter U46619-induced platelet aggregation. Catechol (10–50 µM) suppressed COX-1 activity by 29–44% and COX-2 activity by 29–50%. It also inhibited IL-1β-induced PGE2 production, but not COX-2 expression of fibroblasts. Moreover, catechol (1–10 µM) attenuated AA-induced ROS production in platelets and phorbol myristate acetate (PMA)-induced ROS production in human polymorphonuclear leukocytes. Exposure of platelets to catechol decreased AA-induced ERK and p38 phosphorylation. Finally, intravenous administration of catechol (2.5–5 µmole/mouse) attenuated ex vivo AA-induced platelet aggregation. These results suggest that catechol exhibited anti-platelet and anti-inflammatory effects, which were mediated by inhibition of COX, ROS and TXA2 production as well as ERK/p38 phosphorylation. The anti-platelet effect of catechol was confirmed by ex vivo analysis. Exposure to catechol may affect platelet function and thus cardiovascular health.
Highlights
Various benzenediols are present in many plant-derived products, including vegetables, areca nut, fruits, grains, coffee, tea, beer, and wine [1,2,3]
Materials Catechol, arachidonic acid (AA), U46619, 29,79-diacethyl-chlorofluorescein (DCFH-DA), lactate dehydrogenase (LDH) assay kits, superoxide dismutase (SOD), N-acetyl-L-cysteine (NAC) and sodium citrate were obtained from Sigma
Platelet aggregation assay Washed rabbit platelets were isolated from animals in the Animal Center of National Taiwan University Hospital as previously described [14,15,16] and were suspended in Tyrodes solution containing 1 mM calcium and 0.35% bovine serum albumin (BSA)
Summary
Various benzenediols (e.g., catechol, resorcinol, hydroquinone [HQ]) are present in many plant-derived products, including vegetables, areca nut, fruits, grains, coffee, tea, beer, and wine [1,2,3]. Many catechol (i.e., pyrocatechol) derivatives have been suggested to have therapeutic potential. Phenol and catechol (1,2-benzenediol) are two major metabolites identified in the urine of workers occupationally exposed to benzene. Catechol and HQ (e.g., 1,4-benzenediol) levels in peripheral blood may be a marker of exposure to benzene or cigarette smoke [4]. The effect of catechol on human health remains to be investigated. Catechol scavenges diphenylpicrylhydrazyl radicals and reactive oxygen species (ROS) [5]. Lee and Lin [7] found that catechol, pyrogallol and 1,2,4-benzenetriol may gerenate ROS and exhibit mutagenicity. Catechol and HQ may antagonize transforming growth factor-b (TGF-b)-induced elimination of transformed cells suggesting a co-carcinogenic effect [8]
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