Abstract
Spice active principles are reported to have anti-diabetic, anti-hypercholesterolemic,
antilithogenic, anti-inflammatory, anti-microbial and anti-cancer properties. In our
previous report we have shown that spices and their active principles inhibit 5-lipoxygenase
and also formation of leukotriene C4. In this study, we report the modulatory effect
of spice active principles viz., eugenol, capsaicin, piperine, quercetin, curcumin,
cinnamaldehyde and allyl sulphide on in vitro human platelet aggregation. We have demonstrated that spice active principles inhibit
platelet aggregation induced by different agonists, namely ADP (50μM), collagen (500μg/ml), arachidonic acid (AA) (1.0mM) and calcium ionophore A-23187 (20μM). Spice active principles showed preferential inhibition of arachidonic acid-induced
platelet aggregation compared to other agonists. Among the spice active principles
tested, eugenol and capsaicin are found to be most potent inhibitors of AA-induced
platelet aggregation with IC50 values of 0.5 and 14.6μM, respectively. The order of potency of spice principles in inhibiting AA-induced
platelet aggregation is eugenol>capsaicin>curcumin>cinnamaldehyde>piperine>allyl sulphide>quercetin.
Eugenol is found to be 29-fold more potent than aspirin in inhibiting AA-induced human
platelet aggregation. Eugenol and capsaicin inhibited thromboxane B2 (TXB2) formation
in platelets in a dose-dependent manner challenged with AA apparently by the inhibition
of the cyclooxygenase (COX-1). Eugenol-mediated inhibition of platelet aggregation
is further confirmed by dose-dependent decrease in malondialdehyde (MDA) in platelets.
Further, eugenol and capsaicin inhibited platelet aggregation induced by agonists—collagen,
ADP and calcium ionophore but to a lesser degree compared to AA. These results clearly
suggest that spice principles have beneficial effects in modulating human platelet
aggregation.
Keywords
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Article info
Publication history
Published online: August 25, 2009
Accepted:
April 23,
2009
Received in revised form:
January 7,
2009
Received:
March 7,
2008
Identification
Copyright
© 2009 Elsevier Ltd. Published by Elsevier Inc. All rights reserved.
