化疗药物不同配伍诱导人胰腺癌细胞株细胞凋亡

目的通过对临床常用化疗药物５－氟尿嘧啶（５－ＦＵ）、丝裂霉毒（ＭＭＣ）、卡铂（ＣＢＰ）、阿霉素（ＡＤＭ）和表阿霉素（Ｅ－ＡＤＭ）相互配伍诱导人胰腺癌细胞株细胞凋亡的观察,探讨化疗药物抑制胰腺癌细胞生长的作用机制,为临床制定合理的化疗方案提供理论依据。方法不同配伍的化疗药物作用于胰腺癌细胞后,以倒置显微镜和荧光显微镜观察其形态变化;以流式细胞仪检测细胞ＤＮＡ含量的变化,计算出凋亡细胞的比例;提取细胞ＤＮＡ,进行凝胶电泳确定细胞凋亡的发生。结果联合化疗可以诱导胰腺癌细胞凋亡,与引起细胞坏死相比,诱导肿瘤细胞凋亡的化疗药物剂量小、作用时间短;随作用时间的延长和药物剂量的增加,凋亡细胞的比例也增加;不同配伍的化疗药物诱导不同胰腺癌细胞株细胞发生凋亡的情况是不完全相同的。结论诱导肿瘤细胞凋亡是化疗药物抑制胰腺癌细胞生长的主要机制,能否诱导胰腺癌细胞发生凋亡可作为判断不同配伍的化疗药物抑制胰腺癌细胞生长能力的重要指标之一。

Apoptosis of human pancreatic carcinoma cell lines induced by combinations of chemotherapeutic drugs

Objective To investigate the apoptotic mechanism in human pancreatic carcinoma cell lines P3, SW1990 and Capan 2 induced by the combined treatment of 5 fluorouracil(5FU), mitomycin C (MMC), carboplatin(CBP) or adriamycine (ADM) or epirubicin(E ADM). Methods The changes of cell morphology were monitored by means of microscopic and fluorescence technique after treated with the combinations of chemotherapeutic drugs. The rate of apoptosis was calculated with flow cytometry and the fragmentation of DNA was measured by agarose gel electrophoresis. Results The combinations of chemotherapeutic drugs were able to induce the apoptosis of human pancreatic carcinoma cell lines. Compared with the cell necrosis, the dosage of drugs was less and the time was shorter for inducing apoptosis. With the increased dosage and/or the time prolonged for treating the cells, the rate of apoptotic cells was increased. However, the apoptosis reaction of various human pancreatic carcinoma cell lines, which were mentioned above, induced by the same combinations of chemotherapeutic drugs were various different. Conclusions The apoptosis process might be a mechanism of an inhibiting cancer cell growth induced by the combinations of chemotherapeutic drugs. The examination of apoptosis reaction for the cells induced by different methods and/or chemotherapeutic drugs could become an important index of testing their ability of inhibiting pancreatic neoplasm.