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Protective mechanism of Astragalus Polysaccharides against Cantharidin‐induced liver injury determined in vivo by liquid chromatography/mass spectrometry metabolomics
Author(s) -
Huang Xiaoduo,
Tang Wenchao,
Lin Chang,
Sa Zongge,
Xu Mengdan,
Liu Jieying,
Wang Lina,
Li Wen,
Chen Yunzhi,
Yang Changfu
Publication year - 2021
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.13585
Subject(s) - liver injury , in vivo , metabolomics , cantharidin , pharmacology , ctd , toxicity , glycerophospholipid , metabolism , chemistry , biochemistry , biology , medicine , chromatography , phospholipid , oceanography , microbiology and biotechnology , organic chemistry , membrane , geology
Cantharidin (CTD) is a promising anticancer drug; however, its dosage is limited by hepatotoxicity. We previously showed that Astragalus polysaccharides (APS) effectively improved chemical liver injury. In this study, we established a CTD‐induced subacute liver injury mouse model and examined the effects of APS on weight, liver indexes, histopathology, serum biochemical indexes and liver metabolism. Compared with the control group, mice in the CTD model group had obvious liver damage, which was partially prevented by APS. Metabolomics demonstrated that CTD caused liver damage mainly by regulating glycerophospholipid metabolism, ABC transporter pathways and choline metabolism in cancer in vivo. APS regulated primary bile acid biosynthesis and glycerophospholipid metabolism, thus decreasing the liver damage caused by CTD. This study revealed the protective mechanism of APS against CTD‐induced liver injury from the perspective of metabolomics. The results provide an important basis for analysing the mechanism of CTD‐induced liver toxicity and for assessing clinical treatment options to reduce CTD liver toxicity.