Source:http://linkedlifedata.com/resource/pubmed/id/16445580
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
12
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| pubmed:dateCreated |
2006-1-31
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| pubmed:abstractText |
The aim of the present study was to investigate the effect of prostaglandin (PG) E1 on hypoxia/re-oxygenation (H/R) apoptosis and the expression of bcl-2 and bax in cultured neonatal rat cardiomyocytes. The H/R model was made using the first generation of cultured neonatal rat cardiomyocytes. Hypoxia/re-oxygenation apoptosis was studied by electron microscopy and agarose gel electrophoresis. The percentage of apoptotic cells was measured by terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling (TUNEL). The expression of bcl-2 and bax was detected by in situ hybridization and immunohistochemical staining. Most cells of the H/R group tested by electron microscopy showed cytoplasmic concentration, nuclear chromatin condensation and margination. Prostaglandin E1 (5, 15 and 45 microg/L) relieved the injury. The results of DNA electrophoresis in the H/R group showed a typical DNA ladder and the DNA ladder decreased gradually corresponding with increasing doses of PGE1. The TUNEL staining showed that the total number of apoptotic cells in the H/R group was much more than that in the PGE1 (45 microg/L) group. The results of in situ hybridization and immunohistochemical staining showed that the bcl-2 content in the H/R group was lower than that in the control group; bax content showed the reverse. Compared with the H/R group, bcl-2 content was significantly higher in the PGE1 (5, 15 and 45 microg/L) groups. However, bax content in the PGE1 (5, 15 and 45 microg/L) groups was significantly lower than that in the H/R group. 6. In conclusion, H/R injury can induce cardiomyocyte apoptosis. Prostaglandin E1 obviously has anti-apoptotic effects on cardiomyocytes and the mechanisms probably involve the inhibition of bax expression and increased expression of bcl-2.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Alprostadil,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Oxygen,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
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| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
0305-1870
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
32
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1124-30
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:16445580-Alprostadil,
pubmed-meshheading:16445580-Animals,
pubmed-meshheading:16445580-Animals, Newborn,
pubmed-meshheading:16445580-Anoxia,
pubmed-meshheading:16445580-Apoptosis,
pubmed-meshheading:16445580-Cells, Cultured,
pubmed-meshheading:16445580-DNA,
pubmed-meshheading:16445580-Electrophoresis, Polyacrylamide Gel,
pubmed-meshheading:16445580-Genes, bcl-2,
pubmed-meshheading:16445580-Immunohistochemistry,
pubmed-meshheading:16445580-In Situ Hybridization,
pubmed-meshheading:16445580-In Situ Nick-End Labeling,
pubmed-meshheading:16445580-Microscopy, Electron,
pubmed-meshheading:16445580-Myocytes, Cardiac,
pubmed-meshheading:16445580-Oxygen,
pubmed-meshheading:16445580-RNA, Messenger,
pubmed-meshheading:16445580-Rats,
pubmed-meshheading:16445580-bcl-2-Associated X Protein
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| pubmed:year |
2005
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| pubmed:articleTitle |
Hypoxia-reoxygenation-induced apoptosis in cultured neonatal rat cardiomyocyets and the protective effect of prostaglandin E.
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| pubmed:affiliation |
Department of Pharmacology, College of Basic Sciences, Zhengzhou University, Zhengzhou, China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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