Iran J Basic Med Sci. 2017 Feb;20(2):131-137. doi: 10.22038/ijbms.2017.8235.
Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling.
Iranian journal of basic medical sciences
Xiao-Peng Gao, Dong-Wei Qian, Zhen Xie, Hao Hui
Affiliations
Affiliations
- 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.
- 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.
- Department Two of Neurology, Shaanxi Provincial People's Hospital, Xi'an, China.
PMID: 28293388
PMCID: PMC5339652 DOI: 10.22038/ijbms.2017.8235
Abstract
OBJECTIVES: 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
MATERIALS AND METHODS: An
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.
Keywords: Alcohol; BRL cells; Erk; Hepatotoxicity; Nrf; Oxidative stress
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