中文摘要：

目的探讨镉恶性转化人支气管上皮细胞（16HBE细胞）过程中细胞凋亡状况以及Bal-2和Bax表达变化。方法采用流式细胞术和实时荧光定量PCR法检测16HBE细胞、氯化镉恶性转化16HBE细胞不同阶段（第5、15、35代细胞及成瘤细胞）的细胞凋亡和Bal-2和Bax基因mRNA表达情况。结果 16HBE细胞和恶性转化细胞系第5、15、35代细胞及成瘤细胞的凋亡率分别为0.65%、1.14%、1.87%、3.78%和4.93%;细胞的Bal-2和Bax的mRNA表达量分别为（9.067±0.155）、（8.183±0.206）、（5.971±0.015）、（4.533±0.030）、（4.863±0.066）和（5.973±0.026）、（6.012±0.112）、（6.659±0.028）、（7.032±0.045）、（7.519±0.022）,随着转化代数增加,Bal-2 mRNA表达量逐渐降低,Bax的mRNA表达量逐渐上升,差异均有统计学意义（P〈0.05）。结论氯化镉恶性转化16HBE细胞过程中能引起细胞凋亡,抑止Bal-2基因的表达和上调Bax基因表达。

英文摘要：

Objective To explore the apoptosis and the mRNA expression of Bcl-2 and Bax gene dunng mahgnant transformation of human bronchial epithelial cells（ 16HBE cells） induced by cadmium. Methods Real-time fluorescent quantitative reverse transcriptase polymerase chain reaction（QPCR） was used to detect the level of bal-2 and bax mRNA in 16HBE cells and cell apoptosis of different generations after cadmium chloride exposure（ the 5th, 15th ,35th generation of the cells, and neoplasmed cells from nude mice＇ s tumor tissue）. Flow cytometric analysis was used to analyze cell ap- optosis. Results The apoptosis rates of cadmium chloride exposed 16HBE cells and their 5th,15th,35th generation,and neoplasmed cells from nude mice＇ s tumor tissue were 0. 65 %, 1.14% , 1.87 % , 3.78 % , and 4. 93 %. The relative expres- sion values o f hal-2 mRNA in the 16HBE cells and their 5th, 15th,35th generation, and neoplasmed cells from nude mice＇ s tumor tissue were 9. 067±0. 155,8. 183 ±0. 206,5.971 ± 0. 015, and 4. 533 ±0. 030,4. 863 ± 0. 066, and the relative expression values o f bax mRNA in those cells were 5.973 ±0. 026,6. 012 ±0. 112,6. 659 ±0. 028,7. 032 ±0. 045, and 7. 519 ± 0. 022,respectively. With the increment of transformed generations of 16HBE cells treated with cadmium chloride,the mRNA expression of Bal-2 gene were decreased gradually, while the mRNA expression of Bax gene was increased gradually （P 〈 0. 05 ）. Conclusion Cadmium chloride could induce apoptosis in malignant transformation of human bronchial epithelial cells and down-regulate the expression of hal-2 gene and up-regulate the expression of bax gene.