https://scholars.lib.ntu.edu.tw/handle/123456789/468513
Title: | Gallic acid attenuates platelet activation and platelet-leukocyte aggregation: Involving pathways of Akt and GSK3β | Authors: | Chang S.-S. Lee V.S.Y. Tseng Y.-L. Chang K.-C. Chen K.-B. YUH-LIEN CHEN Li C.-Y. |
Issue Date: | 2012 | Journal Volume: | 2012 | Start page/Pages: | 683872 | Source: | Evidence-based Complementary and Alternative Medicine | Abstract: | Platelet activation and its interaction with leukocytes play an important role in atherothrombosis. Cardiovascular diseases resulted from atherothrombosis remain the major causes of death worldwide. Gallic acid, a major constituent of red wine and tea, has been believed to have properties of cardiovascular protection, which is likely to be related to its antioxidant effects. Nonetheless, there were few and inconsistent data regarding the effects of gallic acid on platelet function. Therefore, we designed this in vitro study to determine whether gallic acid could inhibit platelet activation and the possible mechanisms. From our results, gallic acid could concentration-dependently inhibit platelet aggregation, P-selectin expression, and platelet-leukocyte aggregation. Gallic acid prevented the elevation of intracellular calcium and attenuated phosphorylation of PKCα/p38 MAPK and Akt/GSK3β on platelets stimulated by the stimulants ADP or U46619. This is the first mechanistic explanation for the inhibitory effects on platelets from gallic acid. ? Copyright 2012 Shih-Sheng Chang et al. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84864962166&doi=10.1155%2f2012%2f683872&partnerID=40&md5=dbe72edf63ea50555fd5941506451895 https://scholars.lib.ntu.edu.tw/handle/123456789/468513 |
ISSN: | 1741-427X | DOI: | 10.1155/2012/683872 | SDG/Keyword: | 15 hydroxy 11alpha,9alpha epoxymethanoprosta 5,13 dienoic acid; adenosine diphosphate; calcium; gallic acid; glycogen synthase kinase 3beta; mitogen activated protein kinase p38; PADGEM protein; protein kinase B; protein kinase C alpha; article; calcium cell level; concentration response; drug determination; drug effect; drug mechanism; human; human cell; in vitro study; leukocyte aggregation inhibition; leukocyte function; priority journal; protein expression; protein phosphorylation; thrombocyte aggregation inhibition |
Appears in Collections: | 解剖學暨細胞生物學科所 |
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