NADPH oxidase inhibitor apocynin attenuates ischemia/reperfusion induced myocardial injury in rats / 中华心血管病杂志
Chinese Journal of Cardiology
; (12): 991-996, 2012.
Article
en Zh
| WPRIM
| ID: wpr-292055
Biblioteca responsable:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To explore the role of NADPH oxidase inhibitor apocynin on ischemia/reperfusion (I/R)-induced myocardial injury.</p><p><b>METHODS</b>Male SD rat hearts were divided into the normal control group; sham group; I/R group (1 h ischemia followed by 3 h reperfusion); I/R + apocynin group (50 mg/kg, administrated at 30 min before reperfusion) and I/R + vehicle group (same volume vehicle administrated at 30 min before reperfusion). At the end of reperfusion, myocardial infarct size, apoptosis, plasma CK activity, myocardial NOX activity, myocardial caspase-3 expression and activity, myocardial mRNA and protein expressions of vascular peroxidase 1 (VPO1) and NOX2 were measured.</p><p><b>RESULTS</b>Infarct size, ratio of cardiomyocyte apoptosis, mRNA and protein expression of VOP1 and NOX2, serum CK, myocardial NOX and caspase-3 activities in the I/R group were all significantly increased compared to those in the sham group (P < 0.01). Above parameters were similar between I/R + vehicle group and I/R group (all P > 0.05). Infarct size, ratio of cardiomyocyte apoptosis, myocardial mRNA and protein expression of VOP1 and NOX2, serum CK, myocardial NOX and caspase-3 activities were significantly lower in I/R + apocynin group compared to those in I/R group (all P < 0.01).</p><p><b>CONCLUSIONS</b>NOX/VPO pathway plays an important role in mediating I/R-induced myocardial oxidative injury. NOX inhibition could reduce I/R-induced myocardial oxidative injury by attenuating myocardial apoptosis in this model.</p>
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Base de datos:
WPRIM
Asunto principal:
Oxidación-Reducción
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Acetofenonas
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Peroxidasas
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Farmacología
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Glicoproteínas de Membrana
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Daño por Reperfusión Miocárdica
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Ratas Sprague-Dawley
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Apoptosis
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NADPH Oxidasas
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Quimioterapia
Límite:
Animals
Idioma:
Zh
Revista:
Chinese Journal of Cardiology
Año:
2012
Tipo del documento:
Article