中文摘要：

背景与目的：探讨热休克是否可诱导中国仓鼠肺细胞（CHL）中γH2AX焦点的形成,以及热休克对N-甲基-N＇-硝基-N-亚硝基胍（MNNG）诱导γH2AX焦点形成的影响。材料与方法：用MTT实验检测热休克处理后细胞的生存率,用免疫荧光及流式细胞术检测细胞的γH2AX焦点的形成。结果：MTT结果表明热休克对CHL细胞有细胞毒性作用;免疫荧光实验发现热休克处理后细胞中γH2AX焦点数量与对照组相比无显著差异（P〉0.05）;流式细胞检测结果发现经过热休克预处理再经MNNG处理的细胞与只经过MNNG处理的细胞相比,γH2AX荧光强度由0.316±0.042下降为0.194±0.011,其差异有统计学意义（P〈0.05）。结论：热休克可以使CHL细胞死亡,但是并不引起细胞的遗传毒性;热休克预处理可减少MNNG所诱导的γH2AX焦点的形成。

英文摘要：

BACKGROUND ＆ AIM： To study whether heat shock could induce the formation of γH2AX foci in CHL cells, and the effect of heat shock on N-methyl-N＇＇ -nitro-N-nitrosoguanidine（MNNG） -induced γH2AX loci formation. MATERIALS AND METHODS： The cytotoxic effect of heat shock was evaluated by MTT test. The phosphorylation of γH2AX was assessed using immunofluorescent microscopy and flow cytometry. RESULTS： MTT test showed that heat shock decreased cell viability. There was no significant difference in the number of γH2AX loci between heat-shock treated group and control group as shown by immunofluorescent microscopy. Flow cytometry analysis revealed that pre-heat shock followed by MNNG treatment decreased the mean γH2AX fluorescent intensity from 0.316 ± 0.042 in the MNNG-treatment alone group to 0.194±0.011. CONCLUSION： Heat shock did not induce γH2AX foci formation in CHL cells. In addition, heat shock could inhibit the phosphorylation of H2AX induced by MNNG.