Metabolic regulations of a decoction of Hedyotis diffusa in acute liver injury of mouse models

نویسندگان

  • Min Dai
  • Fenglin Wang
  • Zengcheng Zou
  • Gemin Xiao
  • Hongjie Chen
  • Hongzhi Yang
چکیده

Background Dysfunctional metabolisms are contributed to LPS/GALN-induced hepatitis. However, whether Hedyotis diffusa (HD) employs metabolic strategies against hepatitis is unknown. Methods We use the cytokines expression, levels of serum alanine transaminase and aspartate transaminase, survival and histological analysis to measure the effect of decoction of HD on acute severe hepatitis of mouse induced by LPS/GALN. Meanwhile, we utilize GC/MS-based metabolomics to characterize the variation of metabolomes. Results The present study shows the relieving liver damage in HD decoction-treated mice. Metabolic category using differential metabolites indicates the lower percentage of carbohydrates in LPS/GALN + HD group than LPS/GALN group, revealing the value of carbohydrate metabolism in HD decoction-administrated mouse liver. Further pathway enrichment analysis proposes that citrate cycle, galactose metabolism, and starch and sucrose metabolism are three important carbohydrate metabolisms that involve in the protective effect of decoction of HD during acute hepatitis. Furthermore, other important enrichment pathways are biosynthesis of unsaturated fatty acids, alanine, aspartate and glutamate metabolism, and arginine and proline metabolism. Fatty acids or amino acids involved in above-mentioned pathways are also detected in high loading distribution on IC01 and IC02, thereby manifesting the significance of these metabolites. Other key metabolites detect in ICA analysis were cholesterol, lactic acid and tryptophan. Conclusions The variation tendency of above-mentioned metabolites is totally consistent with the protective nature of decoction of HD. These findings give a viewpoint that HD decoction-effected metabolic strategies are linked to underlying mechanisms of decoction of HD and highlight the importance of metabolic mechanisms against hepatitis.

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عنوان ژورنال:

دوره 12  شماره 

صفحات  -

تاریخ انتشار 2017