[Effect of dehydrocorydaline on formation of thromboxane B2 in platelets and 6-keto-pgf1 alpha in rabbit aorta].
Dehydrocorydaline (DHC) was shown to reduce the production of thromboxane B2 (TXB2) in platelets and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in the aorta of rabbits in vitro. The effect of DHC increased with the increase of dose. DHC 0.41 mg was found to inhibit the formation of TXB2 markedly while not reduce the content of 6-keto-PGF1 alpha. DHC also exhibited obvious inhibitory effect on the arachidonic acid (0.66 mmol/L) induced formation of platelet malondialdehyde (MDA). These effects were similar to the specific cycloxygenase inhibitor, aspirin (0.03 mg/ml). The results suggest that (1) DHC reduced both contents of TXA2 and PGI2 in vitro. (2) DHC markedly inhibited the system of cycloxygenase in cell microsomes. (3) As to whether TXA2 synthetase or cycloxygenase was inhibited in these experiments is still to be elucidated.
Yang
J
J
Wang
Y M
YM
Chai
R H
RH
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D001011:Aorta / Q000378:metabolism; D001792:Blood Platelets / Q000378:metabolism; D002317:Cardiovascular Agents; D008315:Malondialdehyde / Q000097:blood; D011817:Rabbits; D013929:Thromboxane B2 / Q000097:blood
D000470:Alkaloids; D002317:Cardiovascular Agents; C007232:dehydrocorydalin; D008315:Malondialdehyde; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha