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纳米二氧化硅诱导心肌细胞H9c2自噬与凋亡的相互作用及机制

批准号81602893 学科分类卫生毒理 ( H2607 )
项目负责人杜忠君 负责人职称助理研究员 依托单位山东省医学科学院
资助金额18.00
万元
项目类别青年科学基金项目 研究期限2017 年 01 月 01 日 至
2019 年 12 月 31 日
中文主题词纳米二氧化硅;自噬;凋亡;心脏毒性
英文主题词Silica nanoparticles ;Autophagy;Apoptosis;Cardiac toxicity

摘要

中文摘要 纳米二氧化硅作为目前应用最为广泛的纳米材料,其生物安全越来越受到研究者的关注。近年来的研究发现,纳米二氧化硅可以引起心脏毒性。而且细胞凋亡可能是纳米二氧化硅引起心脏毒性的重要机制之一。自噬是细胞内一种溶酶体依赖的细胞内物质进行周转的机制,对生物体正常状态的维持至关重要。多种纳米颗粒都被证明可以引起细胞自噬,并且这种自噬在大多数情况下促进细胞死亡。对于纳米二氧化硅是否能引起心肌细胞自噬,其机制是什么?以及纳米二氧化硅可能引起的自噬对细胞命运有怎样的影响均未见报道。自噬是区别于细胞凋亡的另一种细胞程序性死亡路径,但二者的信号通路在某些环节可能存在交叉。本项目以H9c2细胞为研究模型,深入开展纳米二氧化硅对心肌细胞H9c2细胞自噬和凋亡的影响,并结合二者之间的相互关系及相关机制进行研究,探讨纳米二氧化硅对心肌细胞H9c2自噬的影响以及自噬对细胞命运的作用;并探讨纳米二氧化硅诱导心肌细胞H9c2自噬与凋亡的相互作用;分析beclin1基因在纳米二氧化硅诱导心肌细胞H9c2凋亡中的作用。可为纳米二氧化硅引起心脏毒性的作用机理及对纳米二氧化硅的安全性评价提供新的线索和理论支持。
英文摘要 As the most widely used nanomaterials, silica nanoparticles has attracted more and more attention of researchers. In recent years, many studies have found that silica nanoparticles could cause cardiac toxicity. And apoptosis may be one of the important mechanisms of cardiac toxicity induced by silica nanoparticles. Autophagy is a complex and evolutionarily conserved process. It is involved in the degrading of abnormal proteins and organelles. Autophagy is significant for maintaining cellular homeostasis under regular conditions. A variety of nanoparticles have been shown to induce autophagy, and the elecated autophagy in most of these situations promote cell death. Whether silica nanoparticles could induce autophagy in cardiac muscle cells, and what is the mechanism, and how silica nanoparticles might affect the cell fate have not been reported. Autophagy is another kind of programmed cell death pathway, which is different from apoptosis, but their signaling pathways may cross in some areas. In this project, we will study the effects of silica nanoparticles on autophagy and apoptosis in H9c2 cells. And study on the relationship and the mechanism of autophagy and apoptosis induced silica nanoparticles in H9c2 cell. To investigate the interaction between autophagy and apoptosis of myocardial cells induced by silica nanoparticles, and to analyze the role of Beclin1 gene in the apoptosis of myocardial cells induced, which can provide new clues and theoretical support for the safety evaluation of silica nanoparticles and the mechanism of cardiac toxicity induced by silica nanoparticles.
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