Prevention of colchicine toxicity to cultured rat hepatocytes by glucagon, hydrocortisone and insulin.
Prevention of colchicine toxicity to cultured rat hepatocytes by glucagon, hydrocortisone and insulin.
复制标题
胰高血糖素、氢化可的松和胰岛素预防秋水仙碱对培养大鼠肝细胞的毒性。
DOI：
10.1016/0014-4827(81)90241-x
复制
发表时间：
1981
影响因子：
3.7
通讯作者：
Galivan,J
中科院分区：
文献类型：
--
作者：
Galivan,J
在0.05-0.5 μM浓度范围内，抗微管蛋白剂秋水仙碱可导致原代培养物中大鼠肝细胞脱离。在较低浓度范围（0.02-0.2 μM）下，阿贝斯汀引起相同的效应，但高达1.0 μM的鲁米诺秋水仙碱对细胞无明显影响。提供的数据表明，抗微管蛋白药物的作用具有时间和剂量依赖性。胰高血糖素的存在。氢化可的松和胰岛素可防止秋水仙素引起的细胞脱落。这些成分中的任何一种的遗漏都会导致其他两种在保护秋水仙碱的效果方面无效。长春新碱对细胞的作用部分被相同的组合所阻止。在无血清培养基中进行细胞培养和抗微管蛋白研究，但包含5%胎牛血清不能防止秋水仙素或其他抗微管蛋白剂对细胞的破坏。
The antitubulin agent, colchicine, causes detachment of rat hepatocytes in primary cultures in the concentration range of 0.05–0.5 μM. Vincristine causes the same effect at a lower concentration range (0.02–0.2 μM) but luminocolchicine up to 1.0 μM has no apparent effect on the cells. Data are presented which indicate that the effect of the antitubulin agents is time- as well as dose-dependent. The presence of glucagon. hydrocortisone and insulin prevents the detachment of cells caused by colchicine. Omission of any one of these components causes the other two to be ineffective in protecting against the effect of colchicine. The effect of vincristine on the cells is partially prevented by the same combination. Cell culturing and antitubulin studies were conducted in serum-free medium but the inclusion of 5% fetal bovine serum does not prevent cell destruction by colchicine or other antitubulin agents.