Kometani M, Kanaho Y, Sato T, Fujii T
Eur J Pharmacol. 1985 Apr 23;111(1):97-105. doi: 10.1016/0014-2999(85)90117-7.
Cepharanthine incorporated into rabbit platelets dose dependently, inhibited calcium influx as well as aggregation in response to collagen, and also inhibited arachidonate release in response to collagen and A23187 in the same concentration ranges. The latter action of cepharanthine was shown not to be due to the direct action on phospholipase A2 molecules but to the depression of susceptibility of substrate phospholipids to enzymatic hydrolysis. These depressed functions, as well as the inhibited aggregation, were almost restored by removing the bound drugs from the platelets. Arachidonate-induced aggregation and prostaglandin synthesis from externally added arachidonate were not suppressed by the addition of cepharanthine. These results suggest that cepharanthine physically changes the lipid properties and thereby inhibits the function of the calcium channel or the susceptibility of substrate phospholipids to enzymatic hydrolysis by phospholipase A2.
千金藤素可剂量依赖性地掺入兔血小板中，抑制钙内流以及对胶原的聚集反应，并且在相同浓度范围内还抑制对胶原和A23187的花生四烯酸释放。千金藤素的后一种作用并非由于对磷脂酶A2分子的直接作用，而是由于底物磷脂对酶促水解的敏感性降低。通过从血小板中去除结合的药物，这些受抑制的功能以及受抑制的聚集几乎得以恢复。添加千金藤素不会抑制花生四烯酸诱导的聚集以及从外部添加的花生四烯酸合成前列腺素。这些结果表明，千金藤素可物理性改变脂质特性，从而抑制钙通道功能或底物磷脂对磷脂酶A2酶促水解的敏感性。
