Mitophagy and apoptosis mediated by ROS participate in AlCl3-induced MC3T3-E1 cell dysfunction
Mitophagy and apoptosis mediated by ROS participate in AlCl3-induced MC3T3-E1 cell dysfunction
复制标题
ROS介导的线粒体自噬和细胞凋亡参与AlCl3诱导的MC3T3-E1细胞功能障碍
DOI：
10.1016/j.fct.2021.112388
复制
发表时间：
2021-07-09
影响因子：
4.3
通讯作者：
Li，Yanfei
中科院分区：
文献类型：
--
作者：
Liu，Menglin;Wu，Xia;Li，Yanfei
铝作为一种常见的环境污染物，可引起成骨细胞功能障碍，进而导致铝相关性骨病。ARBD的机制之一是氧化应激，导致活性氧（ROS）产生增加。ROS可引起线粒体损伤，从而诱导线粒体自噬和细胞凋亡。但线粒体自噬和细胞凋亡是否由ROS介导，以及ROS在AlCl 3诱导的MC 3 T3-E1细胞功能障碍中的作用尚不清楚。在本研究中，MC 3 T3-E1细胞使用0 mM Al（对照组）、2 mM Al（Al组）、5 mM N-乙酰半胱氨酸（NAC）（NAC组）、2 mM Al和5 mM NAC（Al + NAC组）24 h。我们发现AlCl 3诱导的MC 3 T3-E1细胞功能障碍伴随着氧化应激、凋亡和线粒体自噬。而活性氧清除剂NAC则能恢复细胞功能，减轻线粒体自噬和凋亡。上述结果提示，ROS介导的线粒体自噬和凋亡参与了AlCl 3诱导的MC 3 T3-E1细胞功能障碍。
Aluminum (Al), as a common environmental pollutant, causes osteoblast (OB) dysfunction and then leads to Al-related bone diseases (ARBD). One of the mechanisms of ARBD is oxidative stress, which leads to an increase in the production of reactive oxygen species (ROS). ROS can induce mitochondrial damage, thereby inducing mitophagy and apoptosis. But whether mitophagy and apoptosis mediated by ROS, and the role of ROS in AlCl3-induced MC3T3-E1 cell dysfunction is still unclear. In this study, MC3T3-E1 cells used 0 mM Al (control group), 2 mM Al (Al group), 5 mM N-acetyl cysteine (NAC) (NAC group), 2 mM Al and 5 mM NAC (Al + NAC group) for 24 h. We found AlCl3-induced MC3T3-E1 cell dysfunction accompanied by oxidative stress, apoptosis, and mitophagy. While NAC, a ROS scavenger treatment, restored cell function and alleviated the mitophagy and apoptosis. These results suggested that mitophagy and apoptosis mediated by ROS participate in AlCl3-induced MC3T3-E1 cell dysfunction.