Protective effect of ATP on skeletal muscle satellite cells damaged by H₂O₂ / 华中科技大学学报(医学)(英德文版)
Journal of Huazhong University of Science and Technology (Medical Sciences)
; (6): 76-81, 2015.
Article
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| WPRIM
| ID: wpr-331105
Biblioteca responsable:
WPRO
ABSTRACT
This study investigated the protective effect of ATP on skeletal muscle satellite cells damaged by H₂O₂in neonatal rats and the possible mechanism. The skeletal muscle satellite cells were randomly divided into four groups: normal group, model group (cells treated with 0.1 mmol/L H₂O₂for 50 s), protection group (cells treated with 16, 8, 4, 2, 1, 0.5, or 0.25 mmol/L ATP for 24 h, and then with 0.1 mmol/L H₂O₂for 50 s), proliferation group (cells treated with 16, 8, 4, 2, 1, 0.5, or 0.25 mmol/L ATP for 24 h). MTT assay, FITC+PI+DAPI fluorescent staining, Giemsa staining and immunofluorescence were performed to examine cell viability and apoptosis, and apoptosis-related proteins. The results showed that the survival rate of skeletal muscle satellite cells was decreased and the apoptosis rate was increased after H₂O₂treatment (P<0.01). Different doses of ATP had different effects on skeletal muscle satellite cells damaged by H₂O₂: the survival rate of muscle satellite cells treated with ATP at 4, 2, or 1 mmol/L was increased. The protective effect was most profound on cells treated with 2 mmol/L ATP. Immunofluorescence showed that ATP could increase the number of Bcl-2-positive cells (P<0.01) and decrease the number of the Bax-positive cells (P<0.01). It was concluded that ATP could protect skeletal muscle satellite cells against H₂O₂damage in neonatal rats, which may be attributed to the up-regulation of the expression of Bcl-2 and down-regulation of Bax, resulting in the suppression of apoptosis.
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Base de datos:
WPRIM
Asunto principal:
Farmacología
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Adenosina Trifosfato
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Ratas Sprague-Dawley
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Células Satélite del Músculo Esquelético
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Peróxido de Hidrógeno
Límite:
Animals
Idioma:
En
Revista:
Journal of Huazhong University of Science and Technology (Medical Sciences)
Año:
2015
Tipo del documento:
Article