title: Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling.
abstract: OBJECTIVE
  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 anin vitrostudy.
  
  
  METHODS
  Anin vitromodel 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department 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.
authors.forename: Xiao-Peng
authors.initials: XP
authors.lastname: Gao
authors.affiliation: Department 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.
authors.forename: Dong-Wei
authors.initials: DW
authors.lastname: Qian
authors.affiliation: Department Two of Neurology, Shaanxi Provincial People's Hospital, Xi'an, China.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Xie
authors.affiliation: Department Two of Neurology, Shaanxi Provincial People's Hospital, Xi'an, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Hui
keywords: Alcohol; BRL cells; Erk; Hepatotoxicity; Nrf; Oxidative stress