摘要
目的 :探讨胶质瘤对化疗药物产生的耐药机制 ,克服耐药性的产生 ,提高化疗效果 ,延缓肿瘤的复发。方法 :模拟临床的给药方法 ,利用VM 2 6在不同条件下的诱导 ,建立了鼠C6胶质瘤细胞株对VM 2 6的耐药模型 ,并通过钙离子拮抗剂尼卡地平、潘生丁的协同作用逆转耐药性。结果 :大剂量、短时间内应用VM 2 6不产生耐药 ,而不同时间从低浓度给药则产生高度耐药。尼卡地平、潘生丁在与VM 2 6协同作用时使VM 2 6对C6 /VM 2 6的抑制率从 33 45 %分别提高到 70 2 5 %、77 6 5 %和 97 0 4%。结论 :肿瘤细胞在短时间内产生的耐药不如逐渐提高剂量的长期药物作用产生的耐药性稳定和显著 ;尼卡地平、潘生丁本身不能抑制肿瘤生长 ,但能通过增强VM 2
Purpose:To study the mechanism of glioma resistance, and to overcome the ocurrence of this resistance, as well as improve the postoporative effect of chemotherapy and delay the recurrence of glioma.Methods:We imitate the way of clinical adminstration and establish a resistant model of C6 cell lines was established as induced by VM 26 and then reversing the resistance through the Nicardipine, Dipyridamole.Results:It was found that the C6 cell line induced by different time dosage groups can produce a stable and high resistance to VM 26. If the C6 cell is induced by the high dosage in a short time, the resistance will not be established. The cell inhibition ratio is enchanced from 33.45% to 70.25 %、77.65 % and 97.04% through using Nicardipine,Dipyridamole.Conclusions:This has indicated that the resistance of different time and dosage inducement is more distinct and stable than the short time inducement. It has been shown that Nicardipine and Dipyridamole alone had no therapeutic effect, but it can enchance the cellular toxicity of VM 26 cell lines and reverse the resistance.
出处
《中国癌症杂志》
CAS
CSCD
2000年第3期216-218,共3页
China Oncology
