摘要
0.5μmol/L CSA与阿霉素联合用药,可显著增强阿霉素对HL-60/Har细胞的毒性。克隆抑制实验证实联合用药时,克隆形成由阿霉素单独用药的155±19降至19±7个,分别是对照的64％和9％,差异显著(P<0.01)。CSA能增加柔红霉素在HL-60/Har细胞内的积累。0.1μ/ml阿霉素对细胞周期没影响。与CSA合用后;阻断于G_2M期的细胞由11％增至50％。结果显示:1.CSA能逆转HL-60/Har细胞的多药抗性;2.逆转作用是通过增加抗肿瘤药物在细胞内的积累来实现的。
Cyclosporins have been shown to sensitive multidrug-resistant cells to chemotherapeutic agents but, generally, have minimal effect on sensitive lines. We studied the effect of cyclos-porin A(CSA) on the action of doxorubicin (DOX), against multidrug resistance HL-60 cells based on proliferation in the present of drug and clone formation in soft-agar. The results suggest that CSA significanily enhanced the cytotoxic effects of DOX. Laser flow cytometry studies on single-cell DAN levels indicated the treatment with DAN in the present of CSA had significantly enhanced cellular accumulation and retention of DAN in resistant cells. Treated with o.lug/ml DOX for 24 hr had no effect on cells' cycle, but, with the synergism of 0.1 ug/ml DOX and 0.5 uM CSA cells were arrested in G2M phase 50% higher than 0.1ug/ml DOX along 11%. These data indicate that increased drug accumulation played aproportionally greater role in the moderately resistant cell line.
出处
《细胞生物学杂志》
CSCD
1995年第1期32-36,共5页
Chinese Journal of Cell Biology
关键词
抗药性
P-糖蛋白
逆转
环孢菌素A
Multidrug resistance P-glycoprotein Reversal Cyclosporin A
