Antiplatelet Activity of α-Lipoic Acid

α-Lipoic acid (ALA) is often used as a dietary supplement to prevent and treat chronic diseases associated with excessive oxidative stress. The aim of this study was to investigate the mechanisms of the antiplatelet activity of ALA. ALA significantly inhibited collagen-induced platelet aggregation,...

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Bibliographic Details
Published in:Journal of agricultural and food chemistry 2010-08, Vol.58 (15), p.8596-8603
Main Authors: Lai, Yuan-Shu, Shih, Ching-Yu, Huang, Yu-Feng, Chou, Tz-Chong
Format: Article
Language:English
Subjects:
Animals
antioxidants
antiplatelet activity
Bioactive Constituents
Biological and medical sciences
blood platelets
Blood Platelets - drug effects
Blood Platelets - enzymology
Blood Platelets - metabolism
collagen
Cyclic AMP - metabolism
Cyclooxygenase 1 - metabolism
dietary supplements
Food industries
Fundamental and applied biological sciences. Psychology
lipoic acid
oxidative stress
platelet aggregation
Platelet Aggregation - drug effects
Platelet Aggregation Inhibitors - pharmacology
prostaglandin synthase
protein kinase C
Rabbits
reactive oxygen species
Reactive Oxygen Species - metabolism
Thioctic Acid - pharmacology
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Summary:α-Lipoic acid (ALA) is often used as a dietary supplement to prevent and treat chronic diseases associated with excessive oxidative stress. The aim of this study was to investigate the mechanisms of the antiplatelet activity of ALA. ALA significantly inhibited collagen-induced platelet aggregation, thromboxane B2 (TXB2) formation, Ca2+ mobilization, and protein kinase Cα (PKCα) activation, but ALA itself increased cyclic AMP formation in rabbit washed platelets. However, the effects of ALA on the above platelet responses were markedly reversed by the addition of 2′5′-ddAdo, an adenylate cyclase inhibitor. Additionally, increased reactive oxygen species (ROS) formation and cyclooxygenase-1 activity stimulated by arachidonic acid were inhibited by ALA. In conclusion, we demonstrated that ALA possesses an antiplatelet activity, which may be associated with an elevation of cyclic AMP formation, involving subsequent inhibition of TXA2, Ca2+ mobilization, and PKCα-mediated pathways. Moreover, inhibition of ROS formation and increase of platelet membrane fluidity may also involve its actions.
ISSN:0021-8561
1520-5118
DOI:10.1021/jf101518p