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作 者:吕华荣[1] 王峻[2] 吴星[1] 周滨音[1] 戴学元[1] 裴永恩[1]
机构地区:[1]湖北省黄石市中心医院神经外科,435000 [2]武汉大学人民医院神经外科
出 处:《中国医药》2012年第8期955-957,共3页China Medicine
摘 要:目的研究苯妥英钠对化学治疗耐药人胶质母细胞瘤细胞(8-MG—BA)内卡莫司汀、替尼泊苷积聚浓度的影响。方法实验细胞分为5组,H4细胞组、8-MG—BA细胞组、8-MG—BA+苯妥英钠5mg/L组、8-MG—BA+苯妥英钠10mg/L组、8-MG—BA+维拉帕米5mg/L组。采用高效液相色谱法(HPLC)检测各组细胞内卡莫司汀、替尼泊苷积聚浓度。采用外标标准曲线法,以药物的质量浓度(C)为横坐标、峰面积(A)为纵坐标进行线性回归计算,并测定仪器精密度与方法回收率。结果吸收1、3h后,H4细胞组细胞内卡莫司汀、替尼泊苷含量均高于8-MG—BA细胞组[吸收1h后卡莫司汀浓度:(1.75±0.05)mg/L比(0.31±0.03)mg/L,吸收3h后卡莫司汀浓度:(1.70±0.03)mg/L比(0.39±0.04)mg/L,吸收1h后替尼泊苷浓度:(1.18±0.03)mg/L比(0.42±0.03)mg/L,吸收3h后替尼泊苷浓度:(1.09±0.04)mg/L比(0.46±0.03)mg/L,均P〈0.01];8-MG—BA+维拉帕米5mg/L组、8-MG—BA+苯妥英钠5mg/L组、8-MG—BA+苯妥英钠10mg/L组细胞内卡莫司汀、替尼泊苷含量均高于8-MG—BA细胞组[吸收1h后卡莫司汀浓度:(0.56±0.04)mg/L、(1.10±0.12)mg/L、(1.37±0.04)mg/L比(0.31±0.03)mg/L,吸收3h后卡莫司汀浓度:(0.68±0.04)mg/L、(1.25±0.03)mg/L、(1.49±0.04)mg/L比(0.39±0.04)mg/L,吸收1h后替尼泊苷浓度:(0.50±0.03)mg/L、(0.59±0.03)mg/L、(0.95±0.04)mg/L比(0.42±0.03)mg/L,吸收3h后替尼泊苷浓度:(0.53±0.04)mg/L、(0.62±0.04)mg/L、(1.01±0.03)mg/L比(0.46±0.03)mg/L,均P〈0.01];8-MG—BA+苯妥英钠5mg/L组、8-MG—BA+苯妥英钠10mg/L组细胞内卡莫司汀、替尼泊苷含量均高于8-MG—BA+维拉帕米5mg/L组(P〈0.01);8-NG—Objective To investigate the concentration of carmustine and teniposide in glioblastoma cell line 8-MG-BA and H4 after incubated in different concentrations of Phenytoin (PHT) in vitro. Methods After treatment with phenytoin on different concentrations, intracellular concentration of carmustine and teniposide in H4 and 8-MG-BA cell line was determined by high efficiency liquid chromatography method in 60 and 120 minutes. Verapamil was used in control group. We used external standard calibration curve method to make linear regression calculations and the instrument precision and recovery rate of the methods were determined. Results The intracellular concentration of of bis-ehloroethyhrosourea (BCNU) and teniposide ( VM-26 ) in H4 cells was significantly higher than that in 8-MG-BA cells in control group ( P 〈 0.01 ). After being treated with PHT 5 rag/L, 10 mg/L and VRP 5 mg/L, the intracellnlar concentration of BCNU and VM-26 in 8-MG-BA cells was significantly higher than that in control group ( P 〈 0.05 ). The intracellular concentration of of BCNU and VM-26 in cells treated with PHT 5 mg/L was significantly lower than that in PHT 10 mg/L treatde group ( P 〈 0.05 ). When the drug mass concentration was 0.05 to 5 mg/L, there was a good linear relationship between drug concentration and peak area. The recovery of VM-26 was (96 ± 5 ) %, ( 100 ± 4 ) % , (99 ± 2) % respectively. The recovery of VM-26 was ( 100 ± 5)%, (99 ±4)%, (99 ±4)% respectively. The intra and inter-day RSD were less than 5% (n =5). Conclusion PHT can increase the intracellrlar concentration of BCNU and VM-26 in 8-MG-BA cells.
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