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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 4820414, 11 pages
Research Article

Baicalin Ameliorates Liver Injury Induced by Chronic plus Binge Ethanol Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and NRF2 in Mice

1Department of Clinical Microbiology and Immunology, Affiliated Hospital of Guizhou Medical University, Guizhou Medical University, Yunyan District, Guiyang City, Guizhou Province 550004, China
2Guizhou Provincial Center for Clinical Laboratory, No. 83 Zhongshandong Road, Guiyang City, China
3Public Health Treatment Center of Guiyang, No. 6 Daying Road, Guiyang City, China
4Department of Infectious Diseases, Affiliated Hospital of Guizhou Medical University, Guiyang City, Guizhou Province 550004, China

Correspondence should be addressed to Yuping Wang

Received 1 April 2017; Revised 7 July 2017; Accepted 12 July 2017; Published 16 August 2017

Academic Editor: Saurabh Chatterjee

Copyright © 2017 Ping He et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Alcoholic liver injury leads to serious complication including death. The potential role of baicalin at the transcription level in mice model of alcohol injury is not known yet. In this study, we examined the effect of baicalin against chronic plus binge ethanol model in mice and understanding the mechanism of protection. Liver function, histology, steatosis, inflammation, NF-κB activity, oxidative stress sources, nuclear translocation of NRF2 transcription factor, and cell death were assessed. Treatment with baicalin ameliorated ethanol-induced oxidative stress, inflammation, and cell death. Baicalin attenuated ethanol-induced proinflammatory molecules such as TNF-α, IL-1β, MIP-2, and MCP-1 and reversed redox-sensitive transcription factor NF-κB activation. Baicalin also modulated Kupffer cell activation in vitro. Baicalin inhibited ethanol-induced expression of reactive oxygen species (ROS) generating enzymes NOX2, p67phox, xanthine oxidase, and iNOS in addition to CYP2E1 activities. Baicalin also enhanced ethanol-induced NRF2 nuclear translocation and increased downstream target gene HO-1 as antioxidant defense. Finally, baicalin reduced significant apoptotic and necrotic cell death. Our study suggests that baicalin ameliorates chronic plus binge ethanol-induced liver injury involving molecular crosstalk of multiple pathways at the transcriptional level and through upregulation of antioxidant defense mechanism.