氯化钴预处理减轻缺氧复氧后大鼠海马神经元的凋亡  被引量:4

CoCl_2 PRETREATING INHIBITS THE APOPTOSIS OF HIPPOCAMPAL NEURONS INDUCED BY HYPOXIA-REOXYGENATION

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作  者:赵彤[1] 于顺[1] 徐艳玲[2] 吴丽颖[2] 马子敏[1] 丁爱石[1] 王福庄[1] 范明[1] 

机构地区:[1]军事医学科学院基础医学研究所神经生物学研究室,北京100850 [2]首都医科大学宣武医院老年病研究所神经化学部,北京100053

出  处:《解剖学报》2003年第5期462-466,共5页Acta Anatomica Sinica

基  金:国家自然科学基金重点资助项目 (39730 190 )

摘  要: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 study the effect of CoCl-2 pretreating on apoptosis of hippocampal neurons induced by hypoxia-reoxygenation. Methods Primary cultured newborn rat hippocampal neurons were treated with CoCl-2.Then,the neurons were exposed to anoxic environment.TUNEL staining method and confocal laser microscope were used to examine separately the apoptotic neurons,intracellular Ca 2+ concentration and mitochodrial membrane potential after anoxic exposure. Results CoCl-2 pretreating greatly decreased the apoptotic neurons induced by acute hypoxia-reoxygenation,and also stabilized the intracellular Ca 2+ concentration and the mitochondrial membrane potential during hypoxic exposure.Conclusion CoCl-2 pretreating protects the apoptosis of hippocampal neurons induced by hypoxia-reoxygenation.The protective effect may relate stabilize the intracellular Ca 2+ concentration and the mitochondrial membrane potential during hypoxia.

关 键 词:氯化钻 预处理 缺氧 复氧 大鼠 海马神经元 凋亡 

分 类 号:Q421[生物学—神经生物学]

 

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