Abstract
In this study, rutaecarpine was tested for its antiplatelet activities in human platelet-rich plasma. In human platelet-rich plasma, rutaecarpine (40-200 μM) inhibited aggregation stimulated by a variety of agonists (i.e., collagen, ADP, adrenaline and arachidonic acid). The antiplatelet activity of rutaecarpine (120 μM) was not significantly attenuated by pretreatment with the nitric oxide synthase inhibitor N(G)-mono-methyl-L-arginine (L-NMMA) (100 μM) or N(G)-nitro-L-arginine methyl ester (L-NAME) (200 μM) and with the guanylyl cyclase inhibitor methylene blue (100 μM). In addition, rutaecarpine (40-200 μM) did not significantly affect cyclic AMP and cyclic GMP levels in human washed platelets, whereas it significantly inhibited thromboxane B2 formation stimulated by collagen (10 μg/ml) and thrombin (0.1 U/ml). Furthermore, rutaecarpine (40-200 μM) inhibited [3H]inositol monophosphate formation stimulated by collagen and thrombin in [3H]myoinositol-loaded platelets. It is concluded that the antiplatelet effects of rutaecarpine are due to inhibition of thromboxane formation and phosphoinositide breakdown.
Original language | English |
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Pages (from-to) | 469-475 |
Number of pages | 7 |
Journal | European Journal of Pharmacology |
Volume | 318 |
Issue number | 2-3 |
DOIs | |
Publication status | Published - Dec 30 1996 |
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Keywords
- Alkaloid
- cAMP
- cGMP
- Phosphoinositide
- Platelet, human
- Rutaecarpine
- Thromboxane A
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Pharmacology
Cite this
Mechanism of inhibition of platelet aggregation by rutaecarpine, an alkaloid isolated from Evodia rutaecarpa. / Sheu, Joen Rong; Hung, Wei Chun; Lee, Yen M.; Yen, Mao Hsiung.
In: European Journal of Pharmacology, Vol. 318, No. 2-3, 30.12.1996, p. 469-475.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mechanism of inhibition of platelet aggregation by rutaecarpine, an alkaloid isolated from Evodia rutaecarpa
AU - Sheu, Joen Rong
AU - Hung, Wei Chun
AU - Lee, Yen M.
AU - Yen, Mao Hsiung
PY - 1996/12/30
Y1 - 1996/12/30
N2 - In this study, rutaecarpine was tested for its antiplatelet activities in human platelet-rich plasma. In human platelet-rich plasma, rutaecarpine (40-200 μM) inhibited aggregation stimulated by a variety of agonists (i.e., collagen, ADP, adrenaline and arachidonic acid). The antiplatelet activity of rutaecarpine (120 μM) was not significantly attenuated by pretreatment with the nitric oxide synthase inhibitor N(G)-mono-methyl-L-arginine (L-NMMA) (100 μM) or N(G)-nitro-L-arginine methyl ester (L-NAME) (200 μM) and with the guanylyl cyclase inhibitor methylene blue (100 μM). In addition, rutaecarpine (40-200 μM) did not significantly affect cyclic AMP and cyclic GMP levels in human washed platelets, whereas it significantly inhibited thromboxane B2 formation stimulated by collagen (10 μg/ml) and thrombin (0.1 U/ml). Furthermore, rutaecarpine (40-200 μM) inhibited [3H]inositol monophosphate formation stimulated by collagen and thrombin in [3H]myoinositol-loaded platelets. It is concluded that the antiplatelet effects of rutaecarpine are due to inhibition of thromboxane formation and phosphoinositide breakdown.
AB - In this study, rutaecarpine was tested for its antiplatelet activities in human platelet-rich plasma. In human platelet-rich plasma, rutaecarpine (40-200 μM) inhibited aggregation stimulated by a variety of agonists (i.e., collagen, ADP, adrenaline and arachidonic acid). The antiplatelet activity of rutaecarpine (120 μM) was not significantly attenuated by pretreatment with the nitric oxide synthase inhibitor N(G)-mono-methyl-L-arginine (L-NMMA) (100 μM) or N(G)-nitro-L-arginine methyl ester (L-NAME) (200 μM) and with the guanylyl cyclase inhibitor methylene blue (100 μM). In addition, rutaecarpine (40-200 μM) did not significantly affect cyclic AMP and cyclic GMP levels in human washed platelets, whereas it significantly inhibited thromboxane B2 formation stimulated by collagen (10 μg/ml) and thrombin (0.1 U/ml). Furthermore, rutaecarpine (40-200 μM) inhibited [3H]inositol monophosphate formation stimulated by collagen and thrombin in [3H]myoinositol-loaded platelets. It is concluded that the antiplatelet effects of rutaecarpine are due to inhibition of thromboxane formation and phosphoinositide breakdown.
KW - Alkaloid
KW - cAMP
KW - cGMP
KW - Phosphoinositide
KW - Platelet, human
KW - Rutaecarpine
KW - Thromboxane A
UR - http://www.scopus.com/inward/record.url?scp=0030607693&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030607693&partnerID=8YFLogxK
U2 - 10.1016/S0014-2999(96)00789-3
DO - 10.1016/S0014-2999(96)00789-3
M3 - Article
C2 - 9016940
AN - SCOPUS:0030607693
VL - 318
SP - 469
EP - 475
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
SN - 0014-2999
IS - 2-3
ER -