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目的 :探讨人肺腺癌A5 49/DDP耐药细胞的多药抗药机理。方法 :应用形态学观察、琼脂糖凝胶电泳、原位DNA断裂点的末端标记法观察细胞凋亡的状况 ,用免疫组化法检测bcl 2基因的表达。结果 :癌细胞在顺铂作用下产生了典型的凋亡形态学改变。 3μg/ml、5 μg/ml、7μg/ml顺铂作用 48小时 ,A5 49细胞DNA裂解片断呈现典型的阶梯状排列条带 ;而在 5 μg/ml、7μg/ml顺铂作用 48小时 ,A5 49/DDP细胞才呈现相似的DNA条带。在 3μg/ml顺铂作用 12小时、18小时、2 4小时 ,A5 49/DDP的凋亡指数分别小于A5 49的凋亡指数。A5 49/DDPbcl 2基因的表达高于A5 49细胞。结论 :A5 49/DDP可抵抗顺铂诱导的细胞凋亡 ,这可能与其细胞bcl 2基因过度表达有关。bcl 2基因过度表达可能是A5 49/DDP细胞抗凋亡及抗药机理之一。
Objective : To explore the multidrug resistance mechanism of human lung adenocarcinoma cell line A5 49/DDP. METHODS: Morphological observations, agarose gel electrophoresis, and in situ DNA fragmentation end-point labeling methods were used to observe the status of cell apoptosis. The expression of bcl 2 gene was detected by immunohistochemistry. RESULTS: Cancer cells produced typical apoptotic morphological changes under the action of cisplatin. At 48 μg of 3 μg/ml, 5 μg/ml, and 7 μg/ml cisplatin, the DNA fragmentation of A5 49 cells showed a typical ladder-like arrangement, and at 5 μg/ml, 7 μg/ml cisplatin for 48 hours, A5 49/DDP cells exhibit similar DNA bands. At 3 μg/ml cisplatin for 12 hours, 18 hours, and 24 hours, the apoptosis index of A5 49/DDP was smaller than that of A5 49, respectively. The expression of A5 49/DDPbcl 2 gene was higher than that of A5 49 cells. Conclusion : A5 49/DDP can resist cisplatin-induced apoptosis, which may be related to its overexpression of bcl 2 gene. Overexpression of bcl 2 gene may be one of the anti-apoptotic and anti-drug mechanisms of A5 49/DDP cells.