三氧化二砷对心肌细胞的毒性及其机制的探讨
poptotic effects of Arsenic trioxide in cardiomyocytes
目的 探讨三氧化二砷（As2O3）对H9c2心肌细胞株凋亡的诱导作用,探讨其机制。方法 H9c2细胞培养，不同浓度As2O3干预后，采用MTT、AO/EB染色法、CaspACE 检测系统观察细胞存活率、形态并检测凋亡。结果As2O3 (2-10μM)使H9c2心肌细胞株活力下降；AO/EB染色法观察可见细胞凋亡的特征形态；caspase-3 阻断剂Ac-DEVD-CHO可以阻断As2O3诱导的凋亡。结论 三氧化二砷诱导的H9c2心肌细胞株凋亡，caspase-3的激活是其所致凋亡的机制之一。
Objective To investigated the toxic mechanisms of Arsenic trioxide (As2O3) in H9c2 cardiomyocytes. Methods The apoptosis cells were detected by MTT assay, AO/EB staining, CaspACE Assay System. Results As2O3 (2-10μM) reduced viability of H9c2 cells and induced morphological and ultrastructural alterations of apoptosis observed by MTT assay and AO/EB staining; increased activation of caspase-3 in As2O3 treated cells. Conclusion These results suggest that As2O3-induced apoptosis of H9c2 cells is mediated, at least in part, by the activation of caspase-3 pathway.
杨宝峰、赵晓燕、吕延杰、柴丽敏
基础医学细胞生物学生物化学
三氧化二砷细胞凋亡caspase-3
rsenic trioxideapoptosiscaspase-3
杨宝峰,赵晓燕,吕延杰,柴丽敏.三氧化二砷对心肌细胞的毒性及其机制的探讨[EB/OL].(2008-03-31)[2025-08-02].http://www.paper.edu.cn/releasepaper/content/200803-943.点此复制
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