Evaluation of the mechanism of Danggui-Shaoyao-San in regulating the metabolome of nephrotic syndrome based on urinary metabonomics and bioinformatics approaches

代谢组 肾病综合征 药理学 医学 代谢途径 新陈代谢 化学 代谢组学 内科学 色谱法 生物化学
作者
Yunlai Wang,Shengnan Fan,Mo Yang,Gaoxiang Shi,Siyao Hu,Dengke Yin,Yazhong Zhang,Fan Xu
出处
期刊:Journal of Ethnopharmacology [Elsevier BV]
卷期号:261: 113020-113020 被引量:16
标识
DOI:10.1016/j.jep.2020.113020
摘要

Danggui-Shaoyao-San (DSS), a well-known classic Traditional Chinese medicine (TCM) formula for enhancing Qi (vital energy and spirit), invigorating blood circulation and promoting diuresis, has been widely used in the treatment of nephrotic syndrome (NS). Previously, we have reported some protective effects of DSS against NS, but the in-depth mechanisms remain unclear. In this study, an ultra performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (UPLC-Q/TOF-MS)-based urinary metabonomics coupled with bioinformatics method was employed to evaluate the mechanisms of DSS in treating NS from the perspective of metabolism. The rat models of NS were established using adriamycin injection. The regulative effects of DSS on NS in rats were first assessed by non-targeted metabonomics, which was based on UPLC-Q/TOF-MS. A series of target prediction models were used to predict the target of components identified in DSS and potential metabolites in NS, combined with the experimental results of metabonomics, to construct the biological network. A total of 16 potential metabolites were screened in NS, of which 13 were significantly regulated by DSS. Metabolic pathway analysis showed that the therapeutic effect of DSS on NS was mainly involved in regulating the amino acid metabolism and energy metabolism. The component-target-metabolites-pathway network revealed 29 targets associated with metabolites that were linked to 27 components of DSS. Bioinformatics analysis showed that the potential targets have various molecular functions (especially serine-type endopeptidase inhibitor activity) and biological process (such as positive regulation of peptidyl-tyrosine phosphorylation or autophosphorylation). The regulation of disrupted metabolic pathways and the relative targets may be the mechanism for DSS in the treatment of NS. Notably, metabonomics coupled with bioinformatics would be useful to explore the mechanism of DSS against NS and provide better insights on DSS for clinical use.
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