最大非毒性剂量汉防己甲素对人鼻咽癌细胞放疗增敏作用的研究

Effects of tetrandrine on enhancing radiosensitivity of human nasopharyngeal carcinoma cells

目的 探讨最大非毒性剂量汉防己甲素（tetrandrine,Tet）对人鼻咽癌细胞株CNE1和CNE2的放射增敏作用.方法 采用单纯放射线照射和Tet联合放射线照射对CNE1和CNE2细胞株进行处理,中性彗星电泳检测不同方式处理组中CNE1和CNE2细胞DNA损伤,流式细胞仪检测细胞周期和细胞凋亡率.结果 单纯放射线照射组CNE1和CNE2细胞平均彗星尾矩（tail moment,TM）分别为（7.13±3.70）（x±s）、（11.52±4.04）,Tet联合放射线照射组平均TM分别为（13.61 ±5.45）、（18.85±6.18）,差异有统计学意义（t值分别为2.784和3.089,P值均＜0.05）.单纯放射线照射组CNE1和CNE2细胞周期以G2期为主,分别为（42.62±2.07）％、（34.82±2.74）％,Tet联合放射线照射组分别为（17.02±1.87）％、（19.64±4.82）％,差异有统计学意义（t值分别为23.173和16.500,P值均＜0.01）.单纯放射线照射组CNE1和CNE2细胞凋亡率分别为（17.24％±0.99）％、（16.68％±0.27）％,Tet联合放射线照射组分别为（19.11±1.24）％、（18.51±2.41）％,差异无统计学意义（P值均＞0.05）.结论 最大非毒性剂量Tet能增加人鼻咽癌细胞株CNE1和CNE2的放射敏感性,其机制可能与去除放射线照射诱导的G2/M期阻滞,降低细胞修复DNA双链断裂能力有关.

Objective To study the effect and mechanism of tetrandrine （Tet） on enhancing radiosensitivity of human nasophayrngeal carcinoma cell lines in vitro.Methods CNE1 and CNE2 were exposed to radiation with or without Tet,the DNA damage of the cells were evaluated by neutral comet electrophoresis,and cell cycle and apoptosis were analyzed by flow cytometry.Results The mean tail movements （TM） of CNE1 treated with radiation or radiation plus Tet were （7.13 ＆#177; 3.70）（x± s） and （13.61 ± 5.45）,respectively （t =2.784,P 〈 0.05）,and TM of CNE2 treated with radiation or radiation plus Tet were （11.52±4.04） and （18.85±6.18）,respectively （t =3.089,P〈0.05）.With the exposure to radiation or radiation plus Tet,the percentages of CNEl in G2 phases were （42.62± 2.07）% and （17.02 ± 1.87） %,respectively （t =23.173,P 〈 0.01）,and the percentages of CNE2 in G2 phases were （34.82± 2.74） % and （19.64± 4.82） %,respectively （t =16.500,P 〈 0.01）.There was no significant difference in the apoptosis rates between the cells treated with radiation or radiation plus Tet regardless of CNE1 （17.24 ± 0.99） % vs （19.11 ± 1.24） %,and CNE2 （16.68 ± 0.27） % vs （18.51 ＆#177; 2.41） % （P 〉 0.05）.Conclusions Tet can enhance radiosensitivity of human nasophayrngeal carcinoma cell lines.The mechanism could be related to abrogation of radiation-induced G2/M arrest and reduction of double-strand break repair capacity.