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UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin
[Image: see text] Dihydromyricetin (DMY), an important flavanone found in Ampelopsis grossedentata, plays a protective role in liver injury. Our previous research found that DMY protected L02 cells against hepatotoxicity caused by emodin. In this study, serum, urine, and liver samples from rats were...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical Society
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7931181/ https://www.ncbi.nlm.nih.gov/pubmed/33681574 http://dx.doi.org/10.1021/acsomega.0c05488 |
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author | Gao, Jian Shi, Ning Guo, Hongju Gao, Junfeng Tang, Xu Yuan, Siyuan Qian, Jiahui Wen, Binyu |
author_facet | Gao, Jian Shi, Ning Guo, Hongju Gao, Junfeng Tang, Xu Yuan, Siyuan Qian, Jiahui Wen, Binyu |
author_sort | Gao, Jian |
collection | PubMed |
description | [Image: see text] Dihydromyricetin (DMY), an important flavanone found in Ampelopsis grossedentata, plays a protective role in liver injury. Our previous research found that DMY protected L02 cells against hepatotoxicity caused by emodin. In this study, serum, urine, and liver samples from rats were systematically used for biochemical analysis, pathological observation, and nontargeted metabolomics to evaluate the toxicity of emodin and DMY intervention. After oral administration of DMY, DMY may alleviate liver injury by improving liver metabolism. Approximately, 8 of 15 metabolites in rat urine and serum were significantly regulated by DMY. Metabolic pathway analysis showed that glutathione metabolism, pyrimidine metabolism, and tryptophan metabolism were the most affected pathways, and 18 proteins were predicted to be potential targets of DMY during the alleviation of liver injury induced by emodin. This research is of great significance in confirming the liver-protective effect of DMY, especially during acute liver injury caused by traditional Chinese medicine. |
format | Online Article Text |
id | pubmed-7931181 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Chemical Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-79311812021-03-05 UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin Gao, Jian Shi, Ning Guo, Hongju Gao, Junfeng Tang, Xu Yuan, Siyuan Qian, Jiahui Wen, Binyu ACS Omega [Image: see text] Dihydromyricetin (DMY), an important flavanone found in Ampelopsis grossedentata, plays a protective role in liver injury. Our previous research found that DMY protected L02 cells against hepatotoxicity caused by emodin. In this study, serum, urine, and liver samples from rats were systematically used for biochemical analysis, pathological observation, and nontargeted metabolomics to evaluate the toxicity of emodin and DMY intervention. After oral administration of DMY, DMY may alleviate liver injury by improving liver metabolism. Approximately, 8 of 15 metabolites in rat urine and serum were significantly regulated by DMY. Metabolic pathway analysis showed that glutathione metabolism, pyrimidine metabolism, and tryptophan metabolism were the most affected pathways, and 18 proteins were predicted to be potential targets of DMY during the alleviation of liver injury induced by emodin. This research is of great significance in confirming the liver-protective effect of DMY, especially during acute liver injury caused by traditional Chinese medicine. American Chemical Society 2021-02-19 /pmc/articles/PMC7931181/ /pubmed/33681574 http://dx.doi.org/10.1021/acsomega.0c05488 Text en © 2021 The Authors. Published by American Chemical Society This is an open access article published under an ACS AuthorChoice License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits copying and redistribution of the article or any adaptations for non-commercial purposes. |
spellingShingle | Gao, Jian Shi, Ning Guo, Hongju Gao, Junfeng Tang, Xu Yuan, Siyuan Qian, Jiahui Wen, Binyu UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin |
title | UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal
the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin |
title_full | UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal
the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin |
title_fullStr | UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal
the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin |
title_full_unstemmed | UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal
the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin |
title_short | UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal
the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin |
title_sort | uplc-q-tof/ms-based metabolomics approach to reveal
the hepatotoxicity of emodin and detoxification of dihydromyricetin |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7931181/ https://www.ncbi.nlm.nih.gov/pubmed/33681574 http://dx.doi.org/10.1021/acsomega.0c05488 |
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