Linked Life Data

18379592

Source:http://linkedlifedata.com/resource/pubmed/id/18379592

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-4-3
pubmed:abstractText
Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. This study assessed the effects of estradiol-17beta (E(2)) (10(-8) M) on hypoxia-induced cell injury and its related signaling in primary cultured chicken hepatocytes. Hypoxic conditions were found to augment the level of DNA damage and to reduce cell viability and the level of [(3)H]-thymidine incorporation, and these phenomena were prevented through treatment with E(2). Hypoxia also increased caspase-3 expression, but showed no evidence of an influence on the expression of Bcl-2. However, E(2) induced an increase in the level of Bcl-2 expression under hypoxic conditions and reduced the level of caspase-3 expression. The effects of E(2) on Bcl-2 and caspase expression were blocked by ICI 182780 (E(2) receptor (ER) antagonist, 10(-7) M). In addition, hypoxia resulted in an increase in the intracellular reactive oxygen species (ROS) generated. These effects were blocked by E(2), but not by E(2)-BSA and ICI 182780. Hypoxia also activated p38 mitogen-activated protein kinase (MAPK), c-JUN N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and nuclear factor-kappaB (NF-kappaB). These effects were blocked by E(2), but not by ICI 182780. The inhibition of p38 MAPK and JNK/SAPK blocked NF-kappaB activation. In conclusion, E(2) was found to protect against hypoxia-induced cell injury in chicken hepatocytes through ER-mediated upregulation of Bcl-2 expression and through reducing the activity of ROS-dependent p38 MAPK, JNK/SAPK and NF-kappaB.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1748-7838
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
491-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18379592-Animals, pubmed-meshheading:18379592-Antioxidants, pubmed-meshheading:18379592-Apoptosis, pubmed-meshheading:18379592-Cell Hypoxia, pubmed-meshheading:18379592-Cells, Cultured, pubmed-meshheading:18379592-Chickens, pubmed-meshheading:18379592-Cytoprotection, pubmed-meshheading:18379592-DNA Fragmentation, pubmed-meshheading:18379592-Endoplasmic Reticulum, pubmed-meshheading:18379592-Enzyme Activation, pubmed-meshheading:18379592-Estradiol, pubmed-meshheading:18379592-Hepatocytes, pubmed-meshheading:18379592-Hydrogen Peroxide, pubmed-meshheading:18379592-Hypoxia-Inducible Factor 1, alpha Subunit, pubmed-meshheading:18379592-Male, pubmed-meshheading:18379592-Mitogen-Activated Protein Kinases, pubmed-meshheading:18379592-NF-kappa B, pubmed-meshheading:18379592-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:18379592-Time Factors, pubmed-meshheading:18379592-Up-Regulation
pubmed:year
2008
pubmed:articleTitle
Estradiol-17beta protects against hypoxia-induced hepatocyte injury through ER-mediated upregulation of Bcl-2 as well as ER-independent antioxidant effects.
pubmed:affiliation
Department of Veterinary Physiology, College of Veterinary Medicine, Biotherapy Human Resources Center (BK21), Chonnam National University, Gwangju 500-757, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't