Antiplatelet effect of catechol is related to inhibition of cyclooxygenase, reactive oxygen species, ERK/p38 signaling and thromboxane A2 production.
Antiplatelet effect of catechol is related to inhibition of cyclooxygenase, reactive oxygen species, ERK/p38 signaling and thromboxane A2 production.
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DOI：
10.1371/journal.pone.0104310
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Jeng JH
中科院分区：
文献类型：
--
作者：
Chang MC;Chang HH;Wang TM;Chan CP;Lin BR;Yeung SY;Yeh CY;Cheng RH;Jeng JH
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.
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影响因子：
11
作者：
Lee, Shern-Fwu;Lin, Jen-Kun
通讯作者：
Lin, Jen-Kun
DOI：
10.1111/j.1432-1033.1994.tb18782.x
发表时间：
1994-04-15
期刊：
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子：
--
作者：
IULIANO, L;PEDERSEN, JZ;VIOLI, F
通讯作者：
VIOLI, F
影响因子：
20.3
作者：
Chang, MC;Lin, HK;Huang, TF
通讯作者：
Huang, TF
影响因子：
4.5
作者：
Mansoor, Saffar;Gupta, Navin;Kenney, M. Cristina
通讯作者：
Kenney, M. Cristina
影响因子：
7.4
作者：
Al Ghouleh, Imad;Khoo, Nicholas K. H.;Knaus, Ulla G.;Griendling, Kathy K.;Touyz, Rhian M.;Thannickal, Victor J.;Barchowsky, Aaron;Nauseef, William M.;Kelley, Eric E.;Bauer, Phillip M.;Darley-Usmar, Victor;Shiva, Sruti;Cifuentes-Pagano, Eugenia;Freeman, Bruce A.;Gladwin, Mark T.;Pagano, Patrick J.
通讯作者：
Pagano, Patrick J.