Abstract |
In experiments on the primary culture of isolated neonatal rat cardiomyocytes it was established that anoxia-reoxygenation activated the process of programmed cell death, apoptosis. The amount of apoptotic cells (defined by fragmentation of a nucleus with Hoechst 33342 staining) during anoxia-reoxygenation was increased in 2.1 fold (P < 0.05). The amount of living and necrotic cells was not changed significantly. Apoptosis of neonatal cardiomyocytes during anoxia-reoxygenation was prevented by activation of ATP-dependent potassium (K( ATP)) channels with diazoxide. Synthesized by us the fluorine-containing analogue of diazoxide had the similar effect: the amount of apoptotic cells was decreased to 3.7% that was similar to control meaning. Application of glybenclamide, which completely abrogated the action of diazoxide and its fluorine-containing analogue, allows us to assert that antiapoptotic effect of the substances mentioned above depends on K( ATP) channels opening.
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Authors | V S Nahibin, V Ie Dosenko, S M Pyvovar, O O Moĭbenko, L M Iahupol's'kyĭ |
Journal | Fiziolohichnyi zhurnal (Kiev, Ukraine : 1994)
(Fiziol Zh (1994))
Vol. 50
Issue 3
Pg. 3-8
( 2004)
ISSN: 2522-9028 [Print] Ukraine |
Vernacular Title | Ftorovanyĭ analoh diazoksydu poperedzhuie apoptoz neonatal'nykh kardiomiotsytiv pid chas anoksiï--reoksyhenatsiï. |
PMID | 15320423
(Publication Type: English Abstract, Journal Article)
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Chemical References |
- Membrane Proteins
- Potassium Channels
- mitochondrial K(ATP) channel
- Fluorine
- Diazoxide
- Oxygen
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Topics |
- Animals
- Animals, Newborn
- Apoptosis
(drug effects)
- Cell Hypoxia
- Cells, Cultured
- Diazoxide
(analogs & derivatives, pharmacology)
- Fluorine
(chemistry)
- Membrane Proteins
(metabolism)
- Models, Biological
- Myocytes, Cardiac
(drug effects, metabolism)
- Oxygen
(pharmacology)
- Potassium Channels
- Rats
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