AI Article Synopsis
- The study examines how nitric oxide (NO), delivered through sodium nitroprusside (SNP), affects cell death (apoptosis) in mouse C2C12 myoblasts using various assays.
- SNP treatment led to observable signs of apoptosis in C2C12 cells, including increased expression of p53 and bax proteins.
- The findings suggest that NO may trigger apoptosis in myoblast cells by activating specific cellular pathways involving p53, bax, and caspase-3.
Article Abstract
To investigate whether nitric oxide (NO) induces apoptosis in myoblast cells, the effect of the sodium nitroprusside (SNP), NO donor, on the apoptosis of mouse C2C12 myoblast cells was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, 4,6-diamidino-2-phenylindole (DAPI) staining, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, DNA fragmentation assay, reverse transcription-polymerase chain reaction (RT-PCR), Western blot analysis, and caspase-3 enzyme assay. Mouse C2C12 myoblast cells treated with SNP exhibited several apoptotic features. SNP increased p53 expression and bax expression. SNP also enhanced caspase-3 enzyme activity. The data show that NO may induce apoptotic cell death in myoblast cells through the activation of p53-, bax-, and caspase-dependent intracellular death-related pathways.
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| http://dx.doi.org/10.1254/jphs.fpj04017x | DOI Listing |
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