摘要
目的:探讨白花丹素(PB)联合术前诱导化疗PF方案对舌癌细胞Tca-8113的化疗增敏作用及其相关机制。方法:体外培养舌癌细胞株Tca-8113,设空白对照组、PB组、顺铂(DDP)组、5氟尿嘧啶(5-Fu)组、PB+DDP组、PB+5-Fu组、PF(DDP+5-Fu)组、PB+PF组。MTT法检测药物对Tca-8113细胞抑制作用,流式细胞术检测细胞凋亡率;Western Blot、ELISA法检测细胞中PI3K、P-AKT蛋白表达水平。结果:PB、DDP、5-Fu对Tca-8113细胞增殖抑制浓度IC10分别为1.35、0.006、0.96μmol/L(培养24 h),依此作为实验浓度;PB联合PF方案较PF方案单独作用,其舌癌细胞的抑制率、早期凋亡率有显著增高(P<0.05)。PB联合PF方案较单独运用PF方案,Tca-8113细胞中PI3K、P-AKT蛋白表达水平显著降低(P<0.05)。结论:PB具有化疗增敏作用,抑制细胞中PI3K/AKT信号通路可能是其主要机制。
Objective: To investigate the effects and relevant mechanism of plumbagin(PB) combined PF preoperative introduction chemotherapy on human tongue cancer Tca-8113 cells. Methods: Tca-8113 cells were cultured in vitro and treated by PB, cisplatin (DDP) ,5-fluorouracil( 5-Fu), PB + DDP, PB + 5-Fu, DDP + 5-Fu (PF) and PB + PF respectively. MTF assay was employed to examine the cell proliferation. Flow cytometry was used to detect the cells apoptosis. Expression of PI3K, P-AKT was assessed by Western Blot and ELISA. Results: The IC10 values of PB, DDP and 5-Fu on Tca-8113 cells were( μmol/L, for 24 h culture) 1.35, 0.006 and 0.96 respectively. PB + PF increased cells inhibition and the apoptosis (P 〈 0.05 ), down-regulated PI3 K and P-AKT ex-pression(P 〈 0.05 ). Conclusion: PB can enhance the chemosensitivity of PF chemotherapy on human tongue cancer Tca-8113 cells. The inhibition of PI3K/AKT signaling pathway might be the main mechanism of the effects.
出处
《实用口腔医学杂志》
CAS
CSCD
北大核心
2014年第3期370-374,共5页
Journal of Practical Stomatology
基金
江西省科技厅科技支撑计划项目(编号:20133BBG70073)