Effect of overexpression of tumor necrosis factor-α in failing heart on contractile function of diaphragm / 中华老年医学杂志
Chinese Journal of Geriatrics
;
(12): 237-240, 2011.
Artículo
en Chino
| WPRIM
| ID: wpr-413893
ABSTRACT
Objective To study the effect of overexpression of tumor necrosis factor-α (TNFα) in failing heart on contractile function of mouse diaphragm. Methods Diaphragms excised from transgenic mice with cardiac specific overexpression of TNF-α and from wild-type littermate controls were studied in vitro with direct electrical stimulation. Cytosolic oxidant levels were measured with 2',7'-dichlorofluorescin diacetate (DCFH-DA). Emissions of the oxidized product were detected by fluorescence microscopy. Results The diaphragm contractile force in transgenic animals with heart failure was 47% less than in controls [(13. 2±0. 8) N/cm2 vs. (25.1±0. 6) N/cm2 , P<O. 01]. The weakness was associated with greater intracellular oxidant levels (P<0. 05) and was partially reversed by 30-minute incubation with the antioxidant N-acetylcysteine (NAC) 10 mmol/L ( P < 0. 01 ).Exogenous TNF-a 500 mmol/L increased oxidant production in diaphragm of wild-type mice and caused weakness that was inhibited by NAC. Conclusions Overexpression of TNF in failing heart causes oxidative stress which leads contractile dysfunction in mouse diaphragm.
Texto completo:
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Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Chinese Journal of Geriatrics
Año:
2011
Tipo del documento:
Artículo
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