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目的 探讨冷冻杀伤肿瘤细胞的分子机制。方法 建立小鼠脑胶质瘤动物模型 ;用末端标记法 (TUNEL)原位检测细胞凋亡 ,DNA琼脂糖电泳观察DNA梯形条带 ;用免疫组织化学ABC法检查bc1 2和bax表达。结果 不同冻融周期作用于G42 2胶质瘤后 ,在不同时间点 ,冷冻灶周边区的肿瘤细胞出现了形态学和DNA水平上的细胞凋亡变化 ,其峰值出现在冷冻后 2 4～ 48h。重复冻融出现更多的凋亡细胞。不同冻融周期均引起冷冻灶周边区细胞bax上调 ,但对抑凋亡基因bc1 2表达无明显影响。结论 冷冻治疗可以诱导G42 2胶质瘤细胞凋亡 ,冷冻诱导的细胞凋亡由bax基因参与介导 ,而与bc1 2表达无关。诱导细胞凋亡可能是冷冻杀伤肿瘤细胞的重要机制。
Objective To investigate the molecular mechanism of freezing and killing tumor cells. Methods Animal models of mouse glioma were established. Apoptosis was detected by TUNEL in situ. The DNA ladder was observed by DNA agarose electrophoresis. The expression of bcl-2 and bax was examined by immunohistochemical ABC method. Results After different freeze-thaw cycles were performed on G42 2 glioma, the apoptosis of the tumor cells in the peripheral region of the freezing zone appeared morphological and DNA changes at different time points. The peak appeared at 24-48 h after freezing . More freeze-thaw cycles appear more apoptotic cells. Different freeze-thaw cycles caused bax up-regulation in the peripheral zone of the freezing stove, but had no significant effect on the expression of the bcl-2. Conclusion Cryotherapy can induce apoptosis of G42 glioma cells, and freezing-induced apoptosis is mediated by bax gene but not bc1 2 expression. Induction of apoptosis may be an important mechanism of freezing and killing tumor cells.