斑蝥素
药理学
谷胱甘肽
代谢组学
脱氧胆酸
化学
肝损伤
色谱法
生物化学
生物
胆汁酸
酶
有机化学
作者
Shisheng Zhu,Lan Ren,Tao Song,Li Zhang,Yalei Dai,Liu Siwen,Peng Zhang
标识
DOI:10.1021/acs.chemrestox.9b00233
摘要
Cantharidin is the major bioactive compound extracted from the blister beetle, a traditional Chinese medicine, and has been proved to be a natural component with widely antitumor activity. However, clinical application of cantharidin is relatively restricted due to its potential toxic effects, especially hepatotoxicity. Although cantharidin-induced liver injury has been reported, the underlying molecular mechanisms remain unclear. In the present study, an UPLC-Q-TOF/MS based metabolomics approach combined with blood biochemical analysis, histopathological examination, and cell apoptosis assay were used to investigate the mechanisms of cantharidin-induced hepatotoxicity. A total of 54 significantly changed metabolites and 14 disturbed metabolic pathways were identified in the cantharidin exposed groups. Among them, four metabolites (oxidized glutathione, glutathione, 3-sulfinoalanine, and deoxycholic acid 3-glucuronide) were selected based on their high impact value and potential biological function in the process of liver injury post cantharidin treatment. Our study provides a deeper understanding of the mechanisms of cantharidin-induced hepatotoxicity and may contribute to reduce the liver injury and gain more effective and safe clinical use of cantharidin. In addition, our results also demonstrated that cantharidin could impair multiple biological processes in liver, and future studies will be necessary to reveal the detailed molecular mechanisms of cantharidin-induced hepatotoxicity.
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