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United States Department of Agriculture

Agricultural Research Service

Title: Caffedymine from cocoa has COX inhibitory activity suppressing the expression of a platelet activation marker, P-Selectin

Author
item Park, Jae

Submitted to: Journal of Agricultural and Food Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 28, 2006
Publication Date: February 1, 2007
Citation: Park, J.B. 2007. Caffedymine from cocoa has COX inhibitory activity suppressing the expression of a platelet activation marker, P-selectin. Journal of Agricultural and Food Chemistry.(6):2171-5.

Interpretive Summary: Platelet activation and consequent biological events are major factors in the development of many cardiovascular and inflammatory diseases such as atherosclerosis, angina, acute myocardial infarction, and ischemic cerebral stroke. P-selectin is a protein which can be found in platelets. Due to significant association of P-selectin with coronary artery diseases and stroke, compounds able to decrease P-selectin presence on platelets have been thoroughly explored. In this study, caffedymine and similar compounds (found in wolfberry, bell pepper, and cocoa seed) have been investigated to determine if they inhibit P-selectin formation in platelets. Caffedymine and N-caffeoyltyramine were found to have potent inhibitory activity, thereby suppressing P-selectin in platelets. These data suggest that such inhibition is likely to be a vital mechanism for biological actions by two compounds, caffedymine and N-caffeoyltyramine. Therefore, the outcomes of this study will provide researchers in nutrition, molecular biology, and medicinal fields new information regarding caffedymine and N-caffeoyltyramine, which would likely reduce the risks of human chronic diseases with fewer adverse effects, compared to current therapy.

Technical Abstract: Caffedymine (N-caffeoyldopamine) is a clovamide-type of phenylpropenoic acid amide found in plants. Previous studies indicate that caffedymine inhibits P-selectin expression on platelets by increasing cAMP through beta-2 adrenoceptors, but the inhibition was only partially repressed by beta-2 adrenoceptor antagonists, suggesting another mechanism underlying the inhibitory effects. Therefore, in this study, the effect of caffedymine and its analogues (N-caffeoyltyramine, N-feruloyltyramine, N-coumaroyltyramine, N-cinnamoyltyramine)on COX enzymes(I and II) was investigated, because COX enzymes are deeply involved in regulating P-selectin expression on human platelets. The decreasing order of COX-I inhibitory activity was caffedymine > N-caffeoyltyramine > N-feruloyltyramine > N-coumaroyltyramine > N-cinnamoyltyramine. Caffedymine was the most potent compound in inhibiting the COX I enzyme. It did so by 43% (P < 0.013), at concentration of 0.01 microM. At the same concentration, caffedymine was also able to inhibit COX-II enzyme by 36% (P < 0.015), and the decreasing order of COX-II inhibitory activity was similar to that of COX I. As a result of the COX inhibition, the amount of thromboxane B2, (thromboxane A2 derivative) also decreased significantly in mouse blood treated with caffedymine and its analogues (0.05 microM). Caffedymine and N-caffeoyltyramine, shown to have potent COX inhibitory activity, were also able to suppress platelet-leukocyte interactions, due to the inhibition of P-selectin expression on platelets. These data indicate that COX inhibition is likely to be another mechanism for caffedymine to inhibit P-selectin expression on platelets.

Last Modified: 9/1/2014
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