State Key Laboratory of Natural Medicines , China Pharmaceutical University , No. 24 Tongjia Lane , Nanjing 210009 , China.
Nanjing Forestry University , Nanjing 210037 , China.
Chem Res Toxicol. 2018 Sep 17;31(9):843-851. doi: 10.1021/acs.chemrestox.8b00066. Epub 2018 Aug 10.
Previous studies have shown that Dioscorea bulbifera rhizome (DBR) can induce hepatotoxicity in clinical practice. However, its underlying mechanisms remain largely unexplored. In the present study, we investigated the global effect of DBR exposure on the proteomic and metabolomic profiles in rats over a 12-week administration using an integrated proteomics and metabolomics approach. The abundance of 1366 proteins and 58 metabolites in the liver of rats after subchronic exposure to DBR was dose-dependently altered. The results indicated that DBR mainly damaged hepatic cells through the aberrant regulation of multiple systems mainly including purine metabolism, pyrimidine metabolism, taurine and hypotaurine metabolism, and bile acid metabolism. Notably, the deregulated proteins including Pnp, Dpyd, Upp1, and Tymp and the differential metabolites including uridine, uracil, cytidine, thymine, adenine, adenosine, adenosine 3'-monophosphate, and deoxycytidine were well correlated to purine and pyrimidine metabolism, which might be novel pathways involved in metabolic abnormalities in rats with DBR-induced liver damage. Collectively, these findings not only contributed to understanding the mechanisms underlying the hepatotoxicity of DBR, but also illustrated the power of integrated proteomics and metabolomics approaches to improve the identification of metabolic pathways and biomarkers indicative of herb-induced liver injury.
先前的研究表明,盾叶薯蓣根茎(DBR)在临床实践中可引起肝毒性。然而,其潜在机制在很大程度上仍未得到探索。在本研究中,我们采用整合蛋白质组学和代谢组学方法,研究了 DBR 暴露在大鼠体内 12 周给药后对蛋白质组和代谢组图谱的整体影响。在亚慢性 DBR 暴露后,大鼠肝脏中 1366 种蛋白质和 58 种代谢物的丰度呈剂量依赖性变化。结果表明,DBR 主要通过多种系统的异常调节,主要包括嘌呤代谢、嘧啶代谢、牛磺酸和牛磺酸代谢以及胆汁酸代谢,来破坏肝细胞。值得注意的是,包括 Pnp、Dpyd、Upp1 和 Tymp 在内的失调蛋白和包括尿嘧啶、尿嘧啶、胞苷、胸腺嘧啶、腺嘌呤、腺苷、腺苷 3'-单磷酸和脱氧胞苷在内的差异代谢物与嘌呤和嘧啶代谢密切相关,这可能是 DBR 诱导的肝损伤大鼠代谢异常的新途径。总之,这些发现不仅有助于理解 DBR 肝毒性的机制,而且还说明了整合蛋白质组学和代谢组学方法在提高与草药诱导肝损伤相关的代谢途径和生物标志物的识别能力方面的作用。