Document Detail

Silibinin inhibits ethanol metabolism and ethanol-dependent cell proliferation in an in vitro model of hepatocellular carcinoma.
MedLine Citation:
PMID:  19900758     Owner:  NLM     Status:  MEDLINE    
Chronic ethanol consumption is a known risk factor for developing hepatocellular carcinoma (HCC). The use of plant-derived antioxidants is gaining increasing clinical prominence as a potential therapy to ameliorate the effects of ethanol on hepatic disease development and progression. This study demonstrates silibinin, a biologically active flavanoid derived from milk thistle, inhibits cytochrome p4502E1 induction, ethanol metabolism and reactive oxygen species generation in HCC cells in vitro. These silibinin-mediated effects also inhibit ethanol-dependent increases in HCC cell proliferation in culture.
Elizabeth Brandon-Warner; James A Sugg; Laura W Schrum; Iain H McKillop
Related Documents :
12131368 - N-acetylcysteine augments the cellular redox changes and cytotoxic activity of internal...
2344868 - Induction of fine structural alteration in cardiac purkinje cells by ischaemic metaboli...
15540798 - Alcohol, oxidative stress, and free radical damage.
15936958 - Oxygen and reactive oxygen species in cartilage degradation: friends or foes?
3467838 - Bone and kidney adenylate cyclase-stimulating activity produced by a hypercalcemic cani...
22553378 - Signaling pathways in cell polarity.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-11-08
Journal Detail:
Title:  Cancer letters     Volume:  291     ISSN:  1872-7980     ISO Abbreviation:  Cancer Lett.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-03-29     Completed Date:  2010-04-16     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  7600053     Medline TA:  Cancer Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  120-9     Citation Subset:  IM    
Copyright Information:
2009 Elsevier Ireland Ltd. All rights reserved.
Department of Biology, The University of North Carolina at Charlotte, 28223, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antioxidants / pharmacology*
Carcinoma, Hepatocellular / metabolism,  pathology*
Cell Line, Tumor
Cell Proliferation / drug effects
Cytochrome P-450 CYP2E1 / genetics
Ethanol / metabolism,  pharmacology*
Lipid Peroxidation / drug effects
Liver Neoplasms, Experimental / metabolism,  pathology*
Mitogen-Activated Protein Kinase 1 / metabolism
Mitogen-Activated Protein Kinase 3 / metabolism
Reactive Oxygen Species / metabolism
Silymarin / pharmacology
Grant Support
Reg. No./Substance:
0/Antioxidants; 0/Reactive Oxygen Species; 0/Silymarin; 4RKY41TBTF/silybin; 64-17-5/Ethanol; EC P-450 CYP2E1; EC Protein Kinase 1; EC Protein Kinase 3

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

Previous Document:  PML3 interacts with TRF1 and is essential for ALT-associated PML bodies assembly in U2OS cells.
Next Document:  Tuning of apoptosis-mediator gene transcription in HepG2 human hepatoma cells through an adenosine s...