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作 者:郭杰[1] 张雯艳[2] 刘忠山[1] 李志超[3] 王铁君[1] 邢程[4]
机构地区:[1]吉林大学第二医院放疗科,长春130041 [2]吉林省妇幼保健院,长春130061 [3]吉林大学公共卫生学院,长春130021 [4]吉林省卫生厅,长春130051
出 处:《中国免疫学杂志》2013年第6期596-599,共4页Chinese Journal of Immunology
基 金:吉林省卫生厅科研基金资助项目(3D5097923427);吉林大学基本科研业务费专项基金资助项目(421030140427);吉林大学青年教师基金资助项目(419070210048)
摘 要:目的:通过观察氯化甲基汞(MMC)诱导大鼠不同发育阶段脑神经细胞凋亡,揭示甲基汞致脑发育损伤的分子机制。方法:建立长期接触低剂量氯化甲基汞致脑发育损伤大鼠动物实验模型。采用荧光标记DNA片段分析试剂盒ApoAlertTM DNA Fragmentation Assay Kit检测长期接触低剂量氯化甲基汞对不同发育阶段仔鼠不同脑区(大脑、小脑和海马)神经元凋亡的影响。结果:实验组和对照组出生后不同时间点仔鼠脑神经元都存在凋亡。随仔鼠脑汞含量的增加,大脑、小脑和海马神经元凋亡均明显增加(P<0.05)。结论:长期接触低剂量氯化甲基汞致脑发育损伤与其诱导神经元过渡凋亡有关。Objective :To study on apoptosis of neuron during development of rat induced by Methylmercury chloride (MMC). Methods: Changes of programmed cell death (PCD) rate of neuron from the cerebra, cerebellum and hippocampus caused by chronic MMC exposure were detected using ApoAlertTM DNA Fragmentation Assay Kit. Results: Apoptosis were seen in developing neurons from both control and experimental groups, however the PCD rates in various experimental groups were significantly higher than that of control group accompanied with the increasing concentration of Hg2+ ( P 〈 0.05 ). Conclusion: The results indicated that there exists a relation- ship between damage in the developing brain and excessive apoptosis of neurons induced by exposure to low doses of MMC chronically.
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