摘要
目的从毒理基因组学角度探讨铅的神经毒性作用机制。方法将体外培养的人神经胶质瘤U251细胞(human U251 glioma cells,U251)分别暴露于浓度为400μg/ml乙酸铅8和24 h,提取RNA。应用cDNA芯片技术筛选差异表达基因,利用信息学技术对MAPK信号通路进行分析。结果 与对照相比,有2840条基因表达发生改变,其中49条差异基因参与MAPK信号通路。结论在本试验条件下,乙酸铅暴露U251细胞后,MAPK信号通路中的重要基因表达发生了显著变化,主要影响P38途径和JNK途径。
Objective To explore the mechanism of neurotoxicity of lead by genomics method.Methods Human U251 glioma cells（U251） were exposed to 400 μg/ml lead acetate for 8h or 24h in vitro.Total RNA samples were extracted and hybridized with Human Genome Array.Bioinformatic tools were used for results analysis.Results Results showed that a total of 2840 transcripts were significantly changed compared to the control sample,49 of those changed genes were involved in MAPK pathway.Conclution The genes that including IL1,IL1R,TNFR,TGFβ,DAXX,MKK6,DDIT3,MAX,MAPK10,NFATC4 regulated by MAPK signaling might be involved in toxicity of lead.Lead maily affected the JNK signaling and P38 signaling.
出处
《毒理学杂志》
CAS
CSCD
北大核心
2010年第5期347-352,共6页
Journal of Toxicology
基金
国家973项目(2002CB512901)
