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Nitric oxide induces apoptosis in mouse C2C12 myoblast cells.

机译:一氧化氮诱导小鼠C2C12成肌细胞凋亡。

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摘要

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.
机译:为研究一氧化氮(NO)是否诱导成肌细胞凋亡,通过3-(4,5-二甲基噻唑-2-基)研究了NO供体硝普钠(SNP)对小鼠C2C12成肌细胞凋亡的影响。 )-2,5-二苯基溴化四氮唑(MTT)测定,流式细胞术,4,6-二mid基-2-苯基吲哚(DAPI)染色,末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记(TUNEL)测定,DNA片段测定,逆转录聚合酶链反应(RT-PCR),蛋白质印迹分析和caspase-3酶检测。用SNP处理的小鼠C2C12成肌细胞具有几种凋亡特征。 SNP增加p53表达和bax表达。 SNP还增强了caspase-3酶的活性。数据表明,NO可能通过激活依赖于p53,bax和caspase的细胞内死亡相关途径来诱导成肌细胞凋亡。

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