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目的 研究类缺血 /再灌注后不同时间点神经元胞质内游离钙离子及神经元凋亡比例变化 ,探讨类缺血 /再灌注后神经元的凋亡与神经内钙离子的关系及氟桂利嗪的治疗意义。方法 利用Ca2 + 指示剂Flu 3/AM作为细胞内钙离子的荧光探针负载培养的神经元 ,共聚焦技术检测细胞内荧光强度的变化 ,原位末端标记法 (TUNEL)观察神经元类缺血再灌注后不同时间点神经元凋亡情况。结果 与类缺血 /再灌注组相比 ,氟桂利嗪对类缺血 /再灌注后神经元胞质内游离钙离子浓度增高和神经元凋亡有显著抑制作用 (P <0 .0 5 ) ;再灌注 3h两组无显著差异。结论 氟桂利嗪可明显抑制类缺血 /再灌注后神经元胞质内钙离子的升高 ,减少神经元凋亡比例。
Objective To study the changes of the ratio of free calcium and neuronal apoptosis in neuronal cytoplasm at different time points after ischemia / reperfusion, to explore the relationship between neuronal apoptosis and neuronal calcium after ischemia / reperfusion Therapeutic significance of cinnarizine. Methods Ca2 + -induced Flu3 / AM was used as a fluorescent probe of intracellular Ca2 + to culture cultured neurons. The changes of intracellular fluorescence intensity were detected by confocal technique. TUNEL was used to observe the neuronal ischemia Neuronal apoptosis at different time points after reperfusion. Results Compared with the ischemia / reperfusion group, flunarizine significantly inhibited the increase of intracellular free calcium concentration and neuronal apoptosis after ischemia / reperfusion (P <0.05) ); 3h after reperfusion no significant difference between the two groups. Conclusion Flunarizine can significantly inhibit the increase of intracellular Ca2 + in neurons after ischemia / reperfusion and decrease the percentage of neuronal apoptosis.