Adenosine protects cardiomyocytes from hypoxia/reoxygenation injury / 生理学报
Acta Physiologica Sinica
; (6): 47-52, 2003.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-318944
Biblioteca responsável:
WPRO
ABSTRACT
The aim of this study was to investigate the protective effect of adenosine (ADO) on cardiomyocytes following hypoxia/reoxygenation (H/R) and its molecular mechanism. Primary cultured cardiomyocytes of neonatal rats were divided into two groups, namely H/R (control) and ADO (1.0 micromol/L) groups. The morphologic changes in cardiomyocytes were observed under an inverted phase-contrast microscope. The following parameters of the two groups were determined lactate dehydrogenase (LDH) activity, intracellular calcium concentration and malondialdehyde (MDA) content. Tumor necrotic factor (TNF-alpha) assay was performed using an ELISA kit and NF-kappaB in the nucleus was analyzed by electrophoretic mobility shift assay (EMSA). The results are as follows (1) after H/R injury, cardiomyocytes contracted, tending to get round in shape and its pseudopods decreased, while marked morphological changes were not observed in ADO group; (2) LDH leakage maintained at a lower level in ADO group than that in the control group during H/R (both P<0.01); (3) ADO significantly reduced the concentration of calcium in cells and prevented calcium overload during H/R (both P<0.01); (4) ADO markedly reduced the content of MDA during H/R (both P<0.01); (5) ADO inhibited the production of TNF-alpha during H/R (both P<0.01); and (6) ADO down-regulated NF-kappaB binding activity of cardiomyocytes during H/R (both P<0.01) The results suggest that (1) exogenous ADO attenuates H/R injury of cultured cardiomyocytes; (2) exogenous ADO inhibits the production of TNF-alpha after H/R injury; (3) exogenous ADO prevents the activation of NF-kappaB, which may be the molecular mechanism of down-regulation of TNF-alpha expression.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Traumatismo por Reperfusão
/
Hipóxia Celular
/
Regulação para Baixo
/
Adenosina
/
Células Cultivadas
/
NF-kappa B
/
Fator de Necrose Tumoral alfa
/
Ratos Sprague-Dawley
/
Biologia Celular
Limite:
Animais
Idioma:
Chinês
Revista:
Acta Physiologica Sinica
Ano de publicação:
2003
Tipo de documento:
Artigo