论文部分内容阅读
目的 研究氯化钴 (CoCl2 )预处理对大鼠海马神经元缺氧 复氧后凋亡的影响及其机制。 方法 用CoCl2 处理原代培养大鼠海马神经元 ,并使其暴露于无氧环境。用TUNEL染色法和激光共聚焦显微镜分别检测缺氧后细胞凋亡率以及细胞线粒体膜电位和胞内游离钙。 结果 CoCl2 预处理明显减少海马神经元在缺氧 复氧后的凋亡数 ,并对急性缺氧期间海马神经元的细胞内Ca2 +浓度和线粒体膜电位具有稳定作用。 结论 CoCl2 预处理对急性缺氧引起的海马神经元凋亡可能具有保护作用 ,其机制可能与其稳定缺氧时细胞内Ca2 +浓度和线粒体膜电位有关。
Objective To investigate the effects of cobalt chloride (CoCl2) pretreatment on the apoptosis of hippocampal neurons after hypoxia-reoxygenation in rats and its mechanism. Methods Primary cultured rat hippocampal neurons were treated with CoCl2 and exposed to anaerobic conditions. TUNEL staining and laser scanning confocal microscopy were used to detect apoptosis rate after hypoxia and mitochondrial membrane potential and intracellular free calcium. Results CoCl2 pretreatment significantly decreased the number of apoptotic hippocampal neurons after hypoxia-reoxygenation and had a stabilizing effect on intracellular Ca2 + concentration and mitochondrial membrane potential in hippocampal neurons during acute hypoxia. Conclusion CoCl2 preconditioning may protect hippocampal neurons from apoptosis induced by acute hypoxia, which may be related to intracellular Ca2 + concentration and mitochondrial membrane potential.