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Schisantherin A alleviated alcohol-induced liver injury by the regulation of alcohol metabolism and NF-kB pathway
Schisantherin A (SinA), one of the most abundant active ingredients of Schisandra chinensis, was reported to protect and benefit the liver, however, its effect on alcohol-induced liver injury (ALI) was still not clear. In the present study, an ALI mice model was induced by feeding mice an alcohol-co...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Japanese Association for Laboratory Animal Science
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6219874/ https://www.ncbi.nlm.nih.gov/pubmed/29806627 http://dx.doi.org/10.1538/expanim.18-0021 |
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author | Li, Bin Li, Dongnan Wang, Yuehua Meng, Xianjun Sun, Xiyun Tian, Jinlong Shi, Lin Ma, Fengming |
author_facet | Li, Bin Li, Dongnan Wang, Yuehua Meng, Xianjun Sun, Xiyun Tian, Jinlong Shi, Lin Ma, Fengming |
author_sort | Li, Bin |
collection | PubMed |
description | Schisantherin A (SinA), one of the most abundant active ingredients of Schisandra chinensis, was reported to protect and benefit the liver, however, its effect on alcohol-induced liver injury (ALI) was still not clear. In the present study, an ALI mice model was induced by feeding mice an alcohol-containing liquid diet for four weeks. Then, 100 mg/kg or 200 mg/kg SinA was administered to mice every day by gavage for the last two weeks. Histopathological analysis showed that alcohol-induced liver lipid vacuoles were reduced by SinA. The activities of aspartate aminotransferase (AST, 61.90 ± 14.65 vs. 93.65 ± 20.50, 50.46 ± 13.21 vs. 93.65 ± 20.50) and alanine transaminase (ALT, 41.29 ± 9.20 vs. 64.04 ± 18.13, 36.52 ± 7.71 vs. 64.04 ± 18.13) in the serum of ALI mice were significantly reduced by 100 mg/kg or 200 mg/kg SinA when compared with control mice. Alcohol-induced oxidative stress and the inflammatory response in the liver were suppressed by SinA in a dose-dependent manner. Meanwhile, treatment with SinA decreased alcohol dehydrogenase (ADH) activity and increased acetaldehyde dehydrogenase (ALDH) activity in ALI mice. Alcohol-induced upregulation of CYP2E1 and CYP1A2 in the liver was inhibited by SinA. Further, SinA suppressed activation of the NF-kB pathway in ALI mice. In conclusion, our findings demonstrate that SinA is able to protect against ALI, and this may be, at least in part, caused by regulation of alcohol metabolism and the NF-kB pathway. Our data suggest a therapeutic potential of SinA in the treatment of ALI. |
format | Online Article Text |
id | pubmed-6219874 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Japanese Association for Laboratory Animal Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-62198742018-11-09 Schisantherin A alleviated alcohol-induced liver injury by the regulation of alcohol metabolism and NF-kB pathway Li, Bin Li, Dongnan Wang, Yuehua Meng, Xianjun Sun, Xiyun Tian, Jinlong Shi, Lin Ma, Fengming Exp Anim Original Schisantherin A (SinA), one of the most abundant active ingredients of Schisandra chinensis, was reported to protect and benefit the liver, however, its effect on alcohol-induced liver injury (ALI) was still not clear. In the present study, an ALI mice model was induced by feeding mice an alcohol-containing liquid diet for four weeks. Then, 100 mg/kg or 200 mg/kg SinA was administered to mice every day by gavage for the last two weeks. Histopathological analysis showed that alcohol-induced liver lipid vacuoles were reduced by SinA. The activities of aspartate aminotransferase (AST, 61.90 ± 14.65 vs. 93.65 ± 20.50, 50.46 ± 13.21 vs. 93.65 ± 20.50) and alanine transaminase (ALT, 41.29 ± 9.20 vs. 64.04 ± 18.13, 36.52 ± 7.71 vs. 64.04 ± 18.13) in the serum of ALI mice were significantly reduced by 100 mg/kg or 200 mg/kg SinA when compared with control mice. Alcohol-induced oxidative stress and the inflammatory response in the liver were suppressed by SinA in a dose-dependent manner. Meanwhile, treatment with SinA decreased alcohol dehydrogenase (ADH) activity and increased acetaldehyde dehydrogenase (ALDH) activity in ALI mice. Alcohol-induced upregulation of CYP2E1 and CYP1A2 in the liver was inhibited by SinA. Further, SinA suppressed activation of the NF-kB pathway in ALI mice. In conclusion, our findings demonstrate that SinA is able to protect against ALI, and this may be, at least in part, caused by regulation of alcohol metabolism and the NF-kB pathway. Our data suggest a therapeutic potential of SinA in the treatment of ALI. Japanese Association for Laboratory Animal Science 2018-05-25 2018 /pmc/articles/PMC6219874/ /pubmed/29806627 http://dx.doi.org/10.1538/expanim.18-0021 Text en ©2018 Japanese Association for Laboratory Animal Science This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/) |
spellingShingle | Original Li, Bin Li, Dongnan Wang, Yuehua Meng, Xianjun Sun, Xiyun Tian, Jinlong Shi, Lin Ma, Fengming Schisantherin A alleviated alcohol-induced liver injury by the regulation of alcohol metabolism and NF-kB pathway |
title | Schisantherin A alleviated alcohol-induced liver injury by the regulation of
alcohol metabolism and NF-kB pathway |
title_full | Schisantherin A alleviated alcohol-induced liver injury by the regulation of
alcohol metabolism and NF-kB pathway |
title_fullStr | Schisantherin A alleviated alcohol-induced liver injury by the regulation of
alcohol metabolism and NF-kB pathway |
title_full_unstemmed | Schisantherin A alleviated alcohol-induced liver injury by the regulation of
alcohol metabolism and NF-kB pathway |
title_short | Schisantherin A alleviated alcohol-induced liver injury by the regulation of
alcohol metabolism and NF-kB pathway |
title_sort | schisantherin a alleviated alcohol-induced liver injury by the regulation of
alcohol metabolism and nf-kb pathway |
topic | Original |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6219874/ https://www.ncbi.nlm.nih.gov/pubmed/29806627 http://dx.doi.org/10.1538/expanim.18-0021 |
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