Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling
Objective(s): Oxidative stress has been established as a key cause of alcohol-induced hepatotoxicity. Licochalcone B, an extract of licorice root, has shown antioxidative properties. This study was to investigate the effects and mechanisms of licochalcone B in ethanol-induced hepatic injury in an in...
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| Format: | Article |
| Language: | English |
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Mashhad University of Medical Sciences
2017-02-01
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| Series: | Iranian Journal of Basic Medical Sciences |
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| Online Access: | http://ijbms.mums.ac.ir/article_8235_cd02bcab4f7a091695514e03be1d07f2.pdf |
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| author | Xiao-peng Gao Dong-wei Qian Zhen Xie Hao Hui |
| author_facet | Xiao-peng Gao Dong-wei Qian Zhen Xie Hao Hui |
| author_sort | Xiao-peng Gao |
| collection | DOAJ |
| description | Objective(s): Oxidative stress has been established as a key cause of alcohol-induced hepatotoxicity. Licochalcone B, an extract of licorice root, has shown antioxidative properties. This study was to investigate the effects and mechanisms of licochalcone B in ethanol-induced hepatic injury in an in vitro study. Materials and Methods: An in vitro model of Ethanol-induced cytotoxicity in BRL cells was used in this study. Cell injury was assessed using WST-1 assay and lactate dehydrogenase, alanine transaminase, and aspartate aminotransferase release assay. Cell apoptosis were quantified by flow cytometric analysis. The intracellular oxidative level was evaluated by reactive oxidative species, malondialdehyde and glutathione detection. Furthermore, the expression level of Erk, p-Erk, Nrf-2 were assessed using Western blot. Results: Treatment with ethanol induced marked cell injury and cell apoptosis in BRL cells. Licochalcone B significantly attenuated ethanol-induced cell injury, and inhibited cell apoptosis. Furthermore, licochalcone B significantly inhibited ethanol-induced intracellular oxidative level, upregulated the expression of p-Erk, and promoted nuclear localization of Nrf2. Additionally, this hepatoprotective role was significantly abolished by inhibition of Erk signaling. However, no apparent effects of Erk inhibition were observed on ethanol-induced hepatotoxicity. Conclusion: This study demonstrates that licochalcone B protects hepatocyte from alcohol-induced cell injury, and this hepatoprotective role might be attributable to apoptosis reduction, inhibition of oxidative stress, and upregulation of Erk–Nrf2. Therefore, licochalcone B might possess potential as a novel therapeutic drug candidate for alcohol-related liver disorders. |
| first_indexed | 2024-04-13T13:25:02Z |
| format | Article |
| id | doaj.art-798af6a83e814eb49a4a87a5e76f69fc |
| institution | Directory Open Access Journal |
| issn | 2008-3866 2008-3874 |
| language | English |
| last_indexed | 2024-04-13T13:25:02Z |
| publishDate | 2017-02-01 |
| publisher | Mashhad University of Medical Sciences |
| record_format | Article |
| series | Iranian Journal of Basic Medical Sciences |
| spelling | doaj.art-798af6a83e814eb49a4a87a5e76f69fc2022-12-22T02:45:10ZengMashhad University of Medical SciencesIranian Journal of Basic Medical Sciences2008-38662008-38742017-02-0120213113710.22038/ijbms.2017.82358235Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signalingXiao-peng Gao0Dong-wei Qian1Zhen Xie2Hao Hui3Department of General Surgery, Xi’an Central Hospital, The Affiliated Xi'an Central Hospital of Xi'an Jiaotong University College of Medicine, Xi'an 710003,P.R.ChinaDepartment of Operation Room, Xi’an Central Hospital, The affiliated Xi'an central hospital of Xi'an Jiaotong university College of Medicine, Xi'an 710003,P.R.ChinaDepartment Two of Neurology, Shaanxi Provincial People’s Hospital, Xi’an, ChinaDepartment Two of Neurology, Shaanxi Provincial People’s Hospital, Xi’an, ChinaObjective(s): Oxidative stress has been established as a key cause of alcohol-induced hepatotoxicity. Licochalcone B, an extract of licorice root, has shown antioxidative properties. This study was to investigate the effects and mechanisms of licochalcone B in ethanol-induced hepatic injury in an in vitro study. Materials and Methods: An in vitro model of Ethanol-induced cytotoxicity in BRL cells was used in this study. Cell injury was assessed using WST-1 assay and lactate dehydrogenase, alanine transaminase, and aspartate aminotransferase release assay. Cell apoptosis were quantified by flow cytometric analysis. The intracellular oxidative level was evaluated by reactive oxidative species, malondialdehyde and glutathione detection. Furthermore, the expression level of Erk, p-Erk, Nrf-2 were assessed using Western blot. Results: Treatment with ethanol induced marked cell injury and cell apoptosis in BRL cells. Licochalcone B significantly attenuated ethanol-induced cell injury, and inhibited cell apoptosis. Furthermore, licochalcone B significantly inhibited ethanol-induced intracellular oxidative level, upregulated the expression of p-Erk, and promoted nuclear localization of Nrf2. Additionally, this hepatoprotective role was significantly abolished by inhibition of Erk signaling. However, no apparent effects of Erk inhibition were observed on ethanol-induced hepatotoxicity. Conclusion: This study demonstrates that licochalcone B protects hepatocyte from alcohol-induced cell injury, and this hepatoprotective role might be attributable to apoptosis reduction, inhibition of oxidative stress, and upregulation of Erk–Nrf2. Therefore, licochalcone B might possess potential as a novel therapeutic drug candidate for alcohol-related liver disorders.http://ijbms.mums.ac.ir/article_8235_cd02bcab4f7a091695514e03be1d07f2.pdfAlcoholBRL cellsErkHepatotoxicityNrfOxidative Stress |
| spellingShingle | Xiao-peng Gao Dong-wei Qian Zhen Xie Hao Hui Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling Iranian Journal of Basic Medical Sciences Alcohol BRL cells Erk Hepatotoxicity Nrf Oxidative Stress |
| title | Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling |
| title_full | Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling |
| title_fullStr | Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling |
| title_full_unstemmed | Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling |
| title_short | Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling |
| title_sort | protective role of licochalcone b against ethanol induced hepatotoxicity through regulation of erk signaling |
| topic | Alcohol BRL cells Erk Hepatotoxicity Nrf Oxidative Stress |
| url | http://ijbms.mums.ac.ir/article_8235_cd02bcab4f7a091695514e03be1d07f2.pdf |
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