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目的研究锌离子螯合剂N-二硫氨基甲酸(DEDTC)对小鼠脑缺血模型海马神经元的影响。方法采用昆明小鼠为实验动物,无创动脉夹夹闭双侧颈总动脉,制备脑缺血再灌注模型。模型动物腹腔注射DEDTC,应用硒化锌AMG染色方法检测模型小鼠海马锌离子分布,应用Caspase-3原位杂交和Western-blot检测模型小鼠海马神经元凋亡。结果 AMG染色结果证实,模型组海马苔藓纤维锌离子比假手术组明显增多,而DEDTC治疗组比模型组明显减少。原位杂交和Western-blot结果表明,与模型组相比,DEDTC治疗组小鼠海马齿状回颗粒细胞Caspase-3阳性反应细胞明显减少,Caspase-3表达下调。结论锌离子螯合剂DEDTC可能对缺血再灌注小鼠海马神经元具有保护作用。
Objective To study the effect of zinc ion chelator N-dithiocarbamic acid (DEDTC) on hippocampal neurons in mouse model of cerebral ischemia. Methods Kunming mice were used as experimental animals, and bilateral common carotid arteries were clipped by noninvasive artery clamp to prepare cerebral ischemia-reperfusion model. The model animals were injected intraperitoneally with DEDTC. The distribution of zinc ion in the hippocampus of model mice was detected by AMG staining method. The apoptosis of hippocampal neurons was detected by Caspase-3 in situ hybridization and Western-blot. Results The results of AMG staining confirmed that mossy fiber zinc ion of hippocampus in model group was significantly increased than that in sham operation group, while DEDTC treatment group was significantly less than model group. In situ hybridization and Western-blot results showed that compared with the model group, Caspase-3 positive cells and the expression of Caspase-3 in the dentate gyrus granule cells in the DEDTC treatment group were significantly decreased. Conclusion DEDTC, a zinc ion chelator, may protect hippocampal neurons from ischemia-reperfusion injury in mice.