Document Detail

Essential roles of ERKs and p38K in up-regulation of GST A1 expression by Maotai content in human hepatoma cell line Hep3B.
MedLine Citation:
PMID:  16786188     Owner:  NLM     Status:  MEDLINE    
It is widely accepted that the consumption of alcohol may lead to hepatic injuries such as hepatic fibrosis and cirrhosis. However, consumption of Maotai, one of the famous liquors in China, is found to have no obvious relevance with hepatic injury as ordinary white wine does in both epidemiological and histopathological studies. Present study used human hepatoma cell line Hep3B to address the mechanisms involved in the resistance of alcohol-induced hepatic injury by Maotai liquor. We found that exposure of Hep3B cells to Maotai residue without ethanol (MRWE) resulted in the increased GST A1 anti-oxidant responsive element (ARE) transcriptional expression, while MRWE treatment did not affect Nrf-2-dependent transcriptional activity. Those findings were further confirmed at all time points and doses tested, suggesting that GST A1 transcription was regulated by MRWE via an Nrf-2-independent pathway. Consistent with GST A1 induction, the phosphorylation of c-Jun, extracellular signal-regulated kinases (ERKs) and p38 kinase (p38 K), were also observed in MRWE-treated Hep3B cells. Furthermore, pretreatment of cells with either PD98059 (an inhibitor specific for MEK1/2-ERKs pathway) or SB202190 (an inhibitor specific for p38 K) led to a significant decrease in the induction of GST A1 transcriptional expression by MRWE treatment. Our results indicate that certain content in MRWE is able to induce GST A1 ARE transcriptional expression, which may provide protective effects for hepatic cells by antagonizing the oxidative stress derived from ethanol via an ERKs- and p38 K-dependent pathway.
Dongyun Zhang; Haitian Lu; Jingxia Li; Xianglin Shi; Chuanshu Huang
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Publication Detail:
Type:  Journal Article     Date:  2006-06-20
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  293     ISSN:  0300-8177     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-11-30     Completed Date:  2007-03-16     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  161-71     Citation Subset:  IM    
Nelson Institute of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA.
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MeSH Terms
Alcoholic Beverages*
Carcinoma, Hepatocellular
Cell Line, Tumor
Dose-Response Relationship, Drug
Extracellular Signal-Regulated MAP Kinases / metabolism*
Glutathione Transferase / genetics*,  metabolism
Liver / enzymology*
Liver Neoplasms
Models, Biological
NF-E2-Related Factor 2 / genetics,  metabolism
Protein-Serine-Threonine Kinases / genetics,  metabolism
Signal Transduction
Time Factors
Transcription Factor AP-1 / genetics,  metabolism
Transcription, Genetic
p38 Mitogen-Activated Protein Kinases / metabolism*
Reg. No./Substance:
0/NF-E2-Related Factor 2; 0/NFE2L2 protein, human; 0/Transcription Factor AP-1; EC protein, human; EC Transferase; EC Kinases; EC Signal-Regulated MAP Kinases; EC Mitogen-Activated Protein Kinases; EC B kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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