The protective effect of DR2 activation on hypoxia/reperfusion injury in the neonatal rat cardiomyocytes and related mechanism / 中国应用生理学杂志
Chinese Journal of Applied Physiology
;
(6): 289-293, 2013.
Artigo
em Chinês
| WPRIM
| ID: wpr-235377
ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of dopamine receptor (DR2) activation on hypoxia/reperfusion injury (HRI) in the neonatal rat cardiomyocytes, and to explore its mechanism.</p><p><b>METHODS</b>The hypoxia/reperfusion (H/R) injury model was established in primarily cultured neonatal rat cardiomyocytes, and randomly assigned control, H/R, bromocriptine (Bro) and haloperidol (Hal) groups. The cell apoptosis was detected using inverted microscope, transmission electron microscope and flow cytometry (FCM). The lactate dehydrogenase(LDH) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in cell medium were analyzed. The expression of mRNA and protein of caspase-3, caspase-8, caspase-9, Fas, Fas-L, Cyt C and Bcl-2 were detected by RT-PCR and Western blot, respectively.</p><p><b>RESULTS</b>Compared with the control group, apoptosis rate, LDH activity, MDA content and the expression of pro-apoptotic factors and anti-apoptotic factors were increased, but SOD activity was decreased in H/R group. Compared with the H/R group, all index above-mentioned were down-regulated or reversed in Bro-group, and had no obvious differences in Hal-group.</p><p><b>CONCLUSION</b>The neonatal rat cardiomyocytes injury and apoptosis caused by hypoxia/reperfusion can be inhibited with DR2 activation, which mechanism is related to scavenging oxygen radical.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Traumatismo por Reperfusão Miocárdica
/
Hipóxia Celular
/
Receptores de Dopamina D2
/
Ratos Wistar
/
Apoptose
/
Estresse Oxidativo
/
Biologia Celular
/
Miócitos Cardíacos
/
Animais Recém-Nascidos
/
Metabolismo
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Applied Physiology
Ano de publicação:
2013
Tipo de documento:
Artigo
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