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Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma
The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism of action in a mouse model of carbon tetrachloride (CCl(4))-induced liver toxicity. Hepatotoxicity was induced in Kunming mice via an intraperitoneal injection (IP) of CCl(4), 10 ml/kg body wei...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647083/ https://www.ncbi.nlm.nih.gov/pubmed/28849019 http://dx.doi.org/10.3892/mmr.2017.7268 |
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author | Han, Jichun Wang, Dong Li, Defang Chen, Xiaoyu Wang, Bo Wang, Fenghua Liu, Xiaona Shang, Jing Zheng, Qiusheng |
author_facet | Han, Jichun Wang, Dong Li, Defang Chen, Xiaoyu Wang, Bo Wang, Fenghua Liu, Xiaona Shang, Jing Zheng, Qiusheng |
author_sort | Han, Jichun |
collection | PubMed |
description | The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism of action in a mouse model of carbon tetrachloride (CCl(4))-induced liver toxicity. Hepatotoxicity was induced in Kunming mice via an intraperitoneal injection (IP) of CCl(4), 10 ml/kg body weight, diluted with corn oil at a 1:500 ratio. LCE was administered once a day for 7 days (IP) as pretreatment at a dose of 5 mg/kg/day. The levels of C-reactive protein (CRP) and tumor necrosis factor (TNF)-α were analyzed to determine the inflammation status. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed using ELISA assays. Liver ultrastructure was observed via optical microscopy. The mRNA and protein expression levels of peroxisome proliferator-activated receptor (PPAR)γ, and nuclear factor (NF)-κB were assayed using quantitative polymerase chain reaction and western blot analysis, respectively. Pretreatment with LCE decreased levels of ALT, AST, CRP and TNF-α, and NF-κB expression in the experimental hepatotoxicity mice model induced by CCl(4). In addition, LCE increased the expression of PPARγ and normalized the hepatic histoarchitecture. However, the effects of LCE were reversed by cotreatment with the PPARγ inhibitor GW9662. The present study suggests that LCE may be used for the treatment of hepatotoxicity, and primarily exhibits its protective role through a PPARγ/NF-κB-mediated pathway. |
format | Online Article Text |
id | pubmed-5647083 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-56470832017-10-24 Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma Han, Jichun Wang, Dong Li, Defang Chen, Xiaoyu Wang, Bo Wang, Fenghua Liu, Xiaona Shang, Jing Zheng, Qiusheng Mol Med Rep Articles The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism of action in a mouse model of carbon tetrachloride (CCl(4))-induced liver toxicity. Hepatotoxicity was induced in Kunming mice via an intraperitoneal injection (IP) of CCl(4), 10 ml/kg body weight, diluted with corn oil at a 1:500 ratio. LCE was administered once a day for 7 days (IP) as pretreatment at a dose of 5 mg/kg/day. The levels of C-reactive protein (CRP) and tumor necrosis factor (TNF)-α were analyzed to determine the inflammation status. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed using ELISA assays. Liver ultrastructure was observed via optical microscopy. The mRNA and protein expression levels of peroxisome proliferator-activated receptor (PPAR)γ, and nuclear factor (NF)-κB were assayed using quantitative polymerase chain reaction and western blot analysis, respectively. Pretreatment with LCE decreased levels of ALT, AST, CRP and TNF-α, and NF-κB expression in the experimental hepatotoxicity mice model induced by CCl(4). In addition, LCE increased the expression of PPARγ and normalized the hepatic histoarchitecture. However, the effects of LCE were reversed by cotreatment with the PPARγ inhibitor GW9662. The present study suggests that LCE may be used for the treatment of hepatotoxicity, and primarily exhibits its protective role through a PPARγ/NF-κB-mediated pathway. D.A. Spandidos 2017-10 2017-08-17 /pmc/articles/PMC5647083/ /pubmed/28849019 http://dx.doi.org/10.3892/mmr.2017.7268 Text en Copyright: © Han et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Han, Jichun Wang, Dong Li, Defang Chen, Xiaoyu Wang, Bo Wang, Fenghua Liu, Xiaona Shang, Jing Zheng, Qiusheng Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma |
title | Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma |
title_full | Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma |
title_fullStr | Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma |
title_full_unstemmed | Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma |
title_short | Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma |
title_sort | licochalcone e protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647083/ https://www.ncbi.nlm.nih.gov/pubmed/28849019 http://dx.doi.org/10.3892/mmr.2017.7268 |
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