Antiplatelet effect of green tea catechins: a possible mechanism through arachidonic acid pathway

Antiplatelet effect of green tea catechins: a possible mechanism through arachidonic acid pathway We have previously reported that green tea catechins (GTC) showed an antithrombotic activity, which might be due to antiplatelet effect rather than anticoagulation. The present study was performed to investigate the effect of GTC on the arachidonic acid (AA) metabolism in order to elucidate a possible antiplatelet mechanism. GTC inhibited the collagen-, AA- and U46619-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC 50 values of 61.0±2.5, 105.0±4.9 and 67.0±3.2 μg/ml, respectively. Moreover, GTC administered orally into rats inhibited the AA-induced platelet aggregation ex vivo by 46.9±6.1% and 95.4±2.2% at the doses of 25 and 50 mg/kg, respectively. ( 3 H)AA liberation induced by collagen in ( 3 H)AA incorporated rabbit platelets was significantly suppressed by GTC compared to the control. GTC also significantly inhibited the thromboxane A 2 (TXA 2 ) and prostaglandin D 2 (PGD 2 ) generations induced by addition of AA in intact rabbit platelets. GTC significantly inhibited TXA 2 synthase activity in a concentration-dependent manner. Moreover, adenosine triphosphate (ATP) release from dense granule was inhibited by GTC in washed platelets. These results suggest that the antiplatelet activity of GTC may be due to the inhibition of TXA 2 formation through the inhibition of AA liberation and TXA 2 synthase. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) Elsevier

Antiplatelet effect of green tea catechins: a possible mechanism through arachidonic acid pathway

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Publisher
Elsevier
Copyright
Copyright © 2004 Elsevier Ltd
ISSN
0952-3278
DOI
10.1016/j.plefa.2003.12.004
Publisher site
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Abstract

We have previously reported that green tea catechins (GTC) showed an antithrombotic activity, which might be due to antiplatelet effect rather than anticoagulation. The present study was performed to investigate the effect of GTC on the arachidonic acid (AA) metabolism in order to elucidate a possible antiplatelet mechanism. GTC inhibited the collagen-, AA- and U46619-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC 50 values of 61.0±2.5, 105.0±4.9 and 67.0±3.2 μg/ml, respectively. Moreover, GTC administered orally into rats inhibited the AA-induced platelet aggregation ex vivo by 46.9±6.1% and 95.4±2.2% at the doses of 25 and 50 mg/kg, respectively. ( 3 H)AA liberation induced by collagen in ( 3 H)AA incorporated rabbit platelets was significantly suppressed by GTC compared to the control. GTC also significantly inhibited the thromboxane A 2 (TXA 2 ) and prostaglandin D 2 (PGD 2 ) generations induced by addition of AA in intact rabbit platelets. GTC significantly inhibited TXA 2 synthase activity in a concentration-dependent manner. Moreover, adenosine triphosphate (ATP) release from dense granule was inhibited by GTC in washed platelets. These results suggest that the antiplatelet activity of GTC may be due to the inhibition of TXA 2 formation through the inhibition of AA liberation and TXA 2 synthase.

Journal

Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA)Elsevier

Published: Jul 1, 2004

References

  • Molecular mechanisms of platelet activation
    Siess, W.
  • Carrageenan and thrombin trigger prostaglandin synthetase-independent aggregation of rabbit platelets
    Vargaftig, B.B.

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