A cigarette component acrolein induces accelerated senescence in human diploid fibroblast IMR-90 cells
A cigarette component acrolein induces accelerated senescence in human diploid fibroblast IMR-90 cells
复制标题
香烟成分丙烯醛诱导人二倍体成纤维细胞 IMR-90 细胞加速衰老
DOI：
10.1007/s10522-013-9454-3
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发表时间：
2013-10-01
期刊：
影响因子：
4.5
通讯作者：
Liu, Jiankang
中科院分区：
文献类型：
--
作者：
Luo, Cheng;Li, Yan;Liu, Jiankang
吸烟导致多种疾病，包括肺癌和心血管疾病，并缩短寿命，尽管其机制尚不清楚。我们假设吸烟可能导致细胞线粒体功能障碍和氧化应激，导致衰老加速。在本研究中，我们测试了丙烯醛（一种主要的代表性吸烟毒物）对人肺成纤维细胞IMR-90细胞在细胞衰老、氧化应激和线粒体功能方面的影响。结果表明，与对照细胞相比，低剂量丙烯醛亚急性处理诱导了以下事件：细胞衰老，表现为β-半乳糖苷酶活性增加，p53和p21表达增加，DNA合成，Sirt1表达减少，端粒长度减少；氧化应激随着活性氧的产生、DNA损伤和蛋白质氧化的增加而发生；线粒体功能障碍表现为线粒体膜电位、线粒体生物发生调节因子PGC-1 α和线粒体复合体I、II、III和v的降低。这些结果表明丙烯醛可能通过增加氧化应激和线粒体功能障碍的机制加速衰老。
Cigarette smoking causes various diseases, including lung cancer and cardiovascular disease, and reduces life span, though the mechanisms are not well understood. We hypothesize that smoking may cause cellular mitochondrial dysfunction and oxidative stress, leading to aging acceleration. In the present study, we tested the effects of acrolein, a major representative smoking toxicant, on human lung fibroblast IMR-90 cells with regard to cellular senescence, oxidative stress, and mitochondrial function. The results showed that subacute treatment with low dose of acrolein induces the following events compared to the control cells: cell senescence demonstrated by increases in the activity of β-galactosidase, the higher expression of p53 and p21, decreases in DNA synthesis, Sirt1 expression, and telomere length; oxidative stress occurred as the increases in the production of reactive oxygen species, DNA damage, and protein oxidation; and mitochondrial dysfunction shown as decreases in the mitochondrial membrane potential, mitochondrial biogenesis regulator PGC-1 alpha and mitochondria complex I, II, III, and V. These results suggest that acrolein may accelerate aging through the mechanism of increasing oxidative stress and mitochondrial dysfunction.