Tsuruo T, Iida H, Tsukagoshi S, Sakurai Y
Cancer Lett. 1981 Jul;13(2):133-7. doi: 10.1016/0304-3835(81)90139-7.
Vinblastine inhibited the growth of cultured KB cells 3 days after drug treatment by 55% and 67% at 2.7 ng/ml and 3.5 ng/ml of the medium, respectively. Lysolecithin and phosphatidylinositol showed only a marginal inhibitory effect on the growth of KB cells at respective concentrations of 35-125 microgram/ml and 50-150 microgram/ml of the medium. Lysolecithin, however, enhanced the cytotoxicity of vinblastine. Depending upon the concentrations of lysolecithin (35-125 microgram/ml), the growth of KB cells was inhibited by 60-91% and 86-98% at respective vinblastine concentrations of 2.7 ng/ml and 3.5 ng/ml. Enhancement of vinblastine-induced cytotoxicity also occurred similarly for phosphatidylinositol. The mechanism could be explained partly by an elevated amount of intracellular vinblastine. Other possible mechanisms can only be speculated.
长春碱在药物处理3天后抑制培养的KB细胞生长,在培养基中浓度为2.7 ng/ml和3.5 ng/ml时,分别抑制55%和67%。溶血卵磷脂和磷脂酰肌醇在培养基中各自浓度为35 - 125微克/毫升和50 - 150微克/毫升时,对KB细胞生长仅显示出微弱的抑制作用。然而,溶血卵磷脂增强了长春碱的细胞毒性。根据溶血卵磷脂的浓度(35 - 125微克/毫升),在长春碱浓度分别为2.7 ng/ml和3.5 ng/ml时,KB细胞生长分别被抑制60 - 91%和86 - 98%。磷脂酰肌醇对长春碱诱导的细胞毒性增强作用也类似。其机制部分可通过细胞内长春碱量的增加来解释。其他可能的机制只能进行推测。