Yang J, Wang Y M, Chai R H
Yao Xue Xue Bao. 1989;24(6):472-5.
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.
脱氢紫堇碱(DHC)在体外可使兔血小板中血栓素B2(TXB2)的生成以及主动脉中6-酮-前列腺素F1α(6-酮-PGF1α)的生成减少。DHC的作用随剂量增加而增强。发现0.41毫克DHC可显著抑制TXB2的形成,而不降低6-酮-PGF1α的含量。DHC对花生四烯酸(0.66毫摩尔/升)诱导的血小板丙二醛(MDA)形成也表现出明显的抑制作用。这些作用与特异性环氧化酶抑制剂阿司匹林(0.03毫克/毫升)相似。结果表明:(1)DHC在体外可降低TXA2和PGI2的含量。(2)DHC显著抑制细胞微粒体中的环氧化酶系统。(3)在这些实验中,究竟是抑制了TXA2合成酶还是环氧化酶仍有待阐明。