混合组学联合生物信息学分析山豆根诱导心脏毒性的作用机制及物质基础

Analysis on Mechanism and Material Basis of Cardiotoxicity Induced by Shandougen(Sophorae Tonkinensis Radix Et Rhizome) by Combination of Mixed Omics and Bioinformatics

目的 混合组学联合生物信息学分析山豆根诱导心脏毒性的作用机制及物质基础。方法 蛋白质组学和代谢组学被用于分析山豆根干预心脏组织后的差异表达蛋白质和代谢物。运用MetaboAnalyst数据库对这些内源性靶点进行联合通路分析。生物信息学数据库被用于筛选毒性靶点和物质基础。结果 混合组学结果表明,经山豆根干预后,小鼠心脏组织中199个蛋白质和12个代谢物发生差异表达。其中,21个差异表达蛋白质参与13个显著调节通路。生物信息学表明,24个成分有可能干预18个毒性靶点的表达。结论 多个靶点参与山豆根诱导的心脏毒性,它们的异常表达有促进心脏疾病和损伤发生的趋势。多种成分有可能成为响应这些作用的物质基础。

Objective By combination of mixed omics and bioinformatics to analyze the mechanism and material basis of the cardiotoxicity induced by Shandougen(Sophorae Tonkinensis Radix Et Rhizome)(ST). Methods Proteomics and metabonomics were used to analyze the differentially expressed proteins and metabolites after treatment with ST. MetaboAnalyst was used for joint pathway analysis. Bioinformatics database was applied to screen the toxic targets and material basis. Results Mixed omics revealed that 199 proteins and 12 metabolites were differentially expressed after the treatment with ST,out of which 21 proteins were significantly enriched in 13 pathways. Bioinformatics showed that 24 compounds may interfere with the expressions of 18 toxic targets of ST. Conclusion Multiple targets were involved in the cardiotoxicity induced by ST,whose dysregulation may show the tendency to promote the occurrence of heart diseases and injury. Multiple compounds may be the toxic material basis in response to these effects.