Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 4، دوره 20، شماره 2، اردیبهشت 2017، صفحه 131-137 اصل مقاله (1.55 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2017.8235 | ||
| نویسندگان | ||
| Xiao-peng Gao* 1؛ Dong-wei Qian2؛ Zhen Xie3؛ Hao Hui3 | ||
| 1Department 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.China | ||
| 2Department 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.China | ||
| 3Department Two of Neurology, Shaanxi Provincial People’s Hospital, Xi’an, China | ||
| چکیده | ||
| 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. | ||
| کلیدواژهها | ||
| Alcohol؛ BRL cells؛ Erk؛ Hepatotoxicity؛ Nrf؛ Oxidative stress | ||
| مراجع | ||
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