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大鼠原代神经细胞放射性损伤敏感性与ROS含量关系及依达拉奉的保护作用 被引量:2

Relationship between the Radiation Injury Sensitivity and the ROS Content in Rat Primary Neural Cell Cultures and the Neuroprotective Effects of Edaravone
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摘要 目的:探讨大鼠原代神经细胞培养体系放射性损伤敏感性与ROS含量关系以及依达拉奉的保护作用。方法:X射线单次照射来源于大鼠海马的原代神经元、星形胶质细胞以及星形胶质细胞-神经元共培养体系,对比评价正常培养或依达拉奉干预与否条件下细胞死亡、凋亡以及活性氧(ROS)含量变化。结果:X射线照射引起原代神经元培养体系ROS含量及细胞死亡率明显升高。共培养体系细胞损伤较轻,星形胶质细胞培养体系则无明显损伤。依达拉奉通过清除ROS可以阻止细胞死亡。结论:放射损伤后,原代神经元培养体系ROS含量明显增高,导致神经元凋亡失调。依达拉奉通过清除ROS逆转这一病理过程而产生神经元保护作用,值得临床推广。 Objective: To study the relationship between the radiation injury sensitivity and the reactive oxygen species (ROS) content in rat primary neural cell cultures and the neuroprotective effects of edaravone. Methods: A single-dose x-ray exposure protocol was used in primary cultures of neurons, astrocytes, and astrocytes-neurons derived from rat hippocampus, with or without edaravone treatment. Cell death, apoptosis and the content of ROS were evaluated. Results: X-ray resulted in significantly raised cell death rate and ROS content in the neuronal cultures. However, the cells injury was lighter in the astrocyte-neuron co-cultures and not significant in the astrocyte cultures. Edaravone inhibits the cell death by eliminating ROS. Conclusion: The content of ROS in neuronal cultures increased significantly after the radiation injury, resulted in apoptosis imbalance of neurons. Edaravone prevents this pathological process by eliminating ROS and thus has a protective effect on neurons, the drug is worth clinical promotion.
出处 《药学与临床研究》 2015年第3期211-216,共6页 Pharmaceutical and Clinical Research
关键词 共培养 放射性损伤 活性氧 依达拉奉 神经保护 Co-culture Radiation injury Reactive oxygen species Edaravone Neuroprotection
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