Protective effect of ATP on skeletal muscle satellite cells damaged by H₂O₂.
10.1007/s11596-015-1392-7
- Author:
Fei FEI
1
;
Dao-li ZHU
;
Li-jun TAO
;
Bao-zhu HUANG
;
Hong-hong ZHANG
Author Information
1. Department of Biology, School of Life Science, Nantong University, Nantong, 226019, China, 13211010019@fudan.edu.cn.
- Publication Type:Journal Article
- MeSH:
Adenosine Triphosphate;
pharmacology;
Animals;
Hydrogen Peroxide;
pharmacology;
Rats;
Rats, Sprague-Dawley;
Satellite Cells, Skeletal Muscle;
drug effects
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2015;35(1):76-81
- CountryChina
- Language:English
-
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.
