| 吴 昂,高 赟.氯喹对阿霉素心脏毒性的保护作用初步研究[J].肿瘤学杂志,2014,20(5):388-392. |
| 氯喹对阿霉素心脏毒性的保护作用初步研究 |
| Preliminary Study on the Protective Effect of Chloroquine on Cardiac Toxicity Induced by Doxorubicin in vitro |
| 投稿时间：2014-01-15 |
| DOI：10.11735/j.issn.1671-170X.2014.05.B008 |
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| 中文关键词: 氯喹 心脏毒性 阿霉素 自噬 心肌细胞 |
| 英文关键词:chloroquine cardiac toxicity doxorubicin autophagy myocardiac cells |
| 基金项目:浙江省医药卫生科技计划（2011KYA033） |
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| 摘要点击次数: 2020 |
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| 中文摘要: |
| 摘 要：［目的］ 探讨自噬抑制剂氯喹对阿霉素所致心肌细胞损伤的保护作用。［方法］ 应用MTT法检测氯喹预处理不同时间后给予不同浓度阿霉素作用24h时的心肌细胞存活率，倒置显微镜观察心肌细胞形态，荧光定量PCR比较氯喹、阿霉素及联合作用对Beclin1表达水平的影响。［结果］ 氯喹可以提高不同浓度阿霉素作用下心肌细胞的存活率，其中氯喹预处理24h可以分别提高低中浓度阿霉素作用下的心肌细胞存活率2.5倍左右，高浓度阿霉素作用下心肌细胞存活率2倍。细胞形态学也显示，同为阿霉素作用下，氯喹预处理可不同程度维持心肌细胞原有正常形态。氯喹可以抑制阿霉素诱导的心肌细胞Beclin1表达水平升高。［结论］ 氯喹对阿霉素引起的心肌细胞损伤有一定的保护作用，可能与其抑制Beclin表达水平有关。 |
| 英文摘要: |
| Abstract：［Purpose］ To investigate the protective effect of autophagy inhibitor chloroquine on myocardiac cells injury induced by doxorubicin. ［Methods］ Myocardiac cells were pretreated with chloroquine for different duration，then the relative survival rates of myocardiac cells incubated with various concentrations of doxorubicin for 24h were detected by MTT assay. The morphous of myocardiac cells between chloroquine group and doxorubicin group were observed by inverted microscope.The expression levels of Beclin1 in chloroquine group，doxorubicin group and combination group were detected by RT-PCR. ［Results］ Chloroquine enhanced the survival rate of myocardiac cells suffered by doxorubicin at different concentrations. When the myocardiac cells were treated with low and median dose doxorubicin，chloroquine pretreated with 24h could enhance 2.5 times of survival rates，similarly，it could increase 2 times of survival rates of myocardiac cells treated with high dose doxorubicin. The morphology of cardiac cells suffered by doxorubicin were maintained in different degrees by chloroquine pretreating. Chloroquine inhibited the increasing expression of Beclin1 induced by doxorubicin. ［Conclusion］ Chloroquine might protect myocardiac cells injury induced by doxorubicin to certain extent，which might relate with its inhibition of Beclin1 expression. |
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