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目的探讨拓扑替康导致拓扑异构酶1(Top1)中毒诱导非分生细胞-神经元凋亡的机制。方法分别用不同浓度、不同作用时间的拓扑替康及不同浓度的博来霉素处理小鼠原代皮层神经元,观察其对神经元的毒性,并利用CCK8法通过OD值的不同计算神经元存活率,然后进行统计学分析,组间差异用单因素方差分析,组内比较用T-test。免疫荧光细胞化学(IF)方法检测γ-H2AX在神经元核内的变化情况,以此来检测DNA单链损伤的程度。结果 CCK-8随着拓扑替康浓度的增高以及作用时间的延长,神经元存活率逐渐降低;随着博来霉素浓度的变化,神经元存活率无明显变化;IF结果显示:随着拓扑替康浓度的增加,核内γ-H2AX量也随之增加。结论拓扑替康能诱导非分生细胞-神经元凋亡。
Objective To investigate the mechanism of Topotecan-induced apoptosis in apomixis-1 (Top1) -induced cells. Methods The primary cortical neurons of mice were treated with topotecan and different concentrations of bleomycin at different concentrations and different time to observe the neurotoxicity of the neurons. CCK8 method was used to calculate the neurons Survival rate, and then for statistical analysis, differences between groups using one-way analysis of variance, intra-group comparison with T-test. The changes of γ-H2AX in neurons were detected by immunofluorescence cytochemistry (IF) method to detect the extent of single-strand DNA damage. Results The survival rate of CCK-8 neurons decreased gradually with the increase of the concentration of topotecan and the prolongation of action time. With the change of bleomycin concentration, the survival rate of neurons showed no significant change. IF results showed that with the increase of topotecan concentration, With the increase of the concentration of Trk, the amount of γ-H2AX in the nucleus also increased. Conclusion Topotecan induces apoptosis of non-meristematic cells - neurons.