Effects and mechanisms of low concentration dopamine on hydrogen peroxide-induced apoptosis in cultured neonatal rat cardiomyocytes / 中国应用生理学杂志
Chinese Journal of Applied Physiology
; (6): 67-71, 2015.
Article
in Zh
| WPRIM
| ID: wpr-243430
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of low concentration dopamine(DA) on hydrogen peroxide-induced apoptosis in cultured rat cardiomyocytes as well as the possible molecular mechanisms.</p><p><b>METHODS</b>Cultured neonatal rat cardiomyocytes were randomly divided into the following groups: control group (control), hydrogen peroxide group (H2O2), pretreated with low concentration dopamine ( DA + H2O2), dopamine receptor l(DR1) antagonist group (DR1 + DA + H2O2), dopamine receptor 2(DR2) antagonist group (DR2 + DA + H2O2). The cell apoptosis was then assessed by MTT and flow cytometry. The cellular ultrastructure changes were observed by transmission electron micro- scope. The activity of lactate dehydrogenase(LDH )and superoxide dismutase (SOD) in cell medium was analyzed by colorimetry. The protein expressions of Cytochrone c, Caspase 3 and Caspase 9 were obtained by Western blot.</p><p><b>RESULTS</b>Compared with hydrogen peroxide group, low concentration dopamine(10 µmol/L) decreased the apoptosis rate and the expression of protein of apoptosis related protein, enhanced SOD activity, decreased LDH activity. DR1 antagonist SCH-23390 treatment inhibited dopamine induced cardiac protective effect. DR2 antagonist haloperido treatment had no changes compared with dopamine group.</p><p><b>CONCLUSION</b>Above findings indicate that low concentration dopanine inhibits apoptosis induced by hydrogen peroxide in neonatal rat cardiomyocytes, which is partly associated with the activation of DR1.</p>
Full text:
1
Database:
WPRIM
Main subject:
Pharmacology
/
Superoxide Dismutase
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Benzazepines
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Dopamine
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Cells, Cultured
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Receptors, Dopamine D1
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Rats, Wistar
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Apoptosis
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Myocytes, Cardiac
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Caspase 3
Limits:
Animals
Language:
Zh
Journal:
Chinese Journal of Applied Physiology
Year:
2015
Document type:
Article