摘要
本文报告以细胞周期特异化疗药长春新碱(VCR)对人脑胶质瘤U251MG细胞进行体外分步诱导法造成细胞的耐药性。细胞集落实验表明,经VCR诱导的胶质瘤细胞U251VR—40在10~40ng/mLVCR培养液中,其细胞形成相当率是未诱导组U251MG细胞的2~13倍(P<0.01)。同时,耐VCR的U251VR—4Q细胞对阿霉素(ADM)亦有交叉耐药性,但与卡氮芥(BCNU)无耐药性产生。另外,5ug/mL尼卡地平(NCDP)能使其反转成药敏细胞。诱导过程中还发现,U251MG胶质瘤细胞直接在高浓度VCR(60ng/mL培养液中被杀伤和发生明显形态变化后,仍有少数细胞在无化疗药培养环境7~10天可以复苏并且再增殖。研究结果不仅表明VCR诱导的胶质瘤细胞能够产生多药耐受性(MDR),而且提示该胶质瘤细胞中可能还存在一种修复微管系统的抗药机理。
Chemotherapeutic resistance in U251MG human glioma cells was caused by the step-wise
revulsion with a cell cycle specific agent vincristine(VCR)in vitro。 he cell cloning
experimentdemonstrated that the colony-forming efficency of U251V ̄R--40 cells induced
stepwisely in VCR was2 to 13 folds that of U251MG cells without inducement,in cell culture with
10~40 ng/mL VCR(P<0.01 ).Simultaneously,the cross-resistance to adriamycin(ADM)and no
resistance to BCNU wereappeared in U251V ̄R--40 cells。 However,the resistance cells could
be reversed into the drug--sensi-tive cells by 5.Oμg/mL nicardipine(NCDP).In addition,it was
observed that some cells with mopho-logic change might resuscitate and remultiply in no drug
culture for 10 days later,while most of cellswere killed after U251MG cells were incubated
directly in higher dose of VCR(60 ng/mL).Thisstudy not only revealed that the glioma cells
could produce multidrug resistance(MDR)after VCR in-ducement,but also suggested that
another mechanism of drug resistance,which repaired microtublesystem,might be in the glioma
cells。
出处
《白求恩医科大学学报》
CSCD
1995年第6期590-593,共4页
Journal of Norman Bethune University of Medical Science
基金
吉林省卫生厅科研招标课题资助