Shi Xiaolan, Wei Wenfeng, Wang Ning
Department of Respiratory and Asthma, Xi'an Children's Hospital, Xi'an, Shanxi 710043, P.R. China.
Department of Paediatrics, Xianyang Central Hospital, Xi'an, Shanxi 712000, P.R. China.
Oncol Lett. 2018 Jun;15(6):9609-9616. doi: 10.3892/ol.2018.8554. Epub 2018 Apr 23.
In the present study, the role of in cellular apoptosis and autophagy induced by lipopolysaccharide (LPS) in human epithelial A549 lung-cancer cells was investigated. Initially, it was demonstrated that LPS attenuated A549 cell viability in a time- and dose-dependent manner. Furthermore, LPS induced apoptotic cell death and autophagy in A549 cells and increased reactive oxygen species (ROS) production in a time-dependent manner. In addition, LPS treatment was demonstrated to markedly suppress sirtuin 1 (SIRT1) protein expression in A549 cells. Notably, it was demonstrated that polysaccharides activate SIRT1, leading to increased p62 expression, decreased p53 acetylation and B-cell lymphoma 2-associated X protein expression, and subsequently attenuate LPS-induced apoptotic cell death and autophagy. The results of the present study demonstrated that polysaccharides activate SIRT1 and inhibit LPS-induced ROS production, apoptosis and autophagy. This may have critical implications for the treatment of infection.
在本研究中，研究了[具体物质]在人上皮性A549肺癌细胞中由脂多糖（LPS）诱导的细胞凋亡和自噬中的作用。最初，证明LPS以时间和剂量依赖性方式减弱A549细胞活力。此外，LPS诱导A549细胞凋亡性细胞死亡和自噬，并以时间依赖性方式增加活性氧（ROS）的产生。此外，证明LPS处理可显著抑制A549细胞中沉默调节蛋白1（SIRT1）的蛋白表达。值得注意的是，证明[具体物质]多糖激活SIRT1，导致p62表达增加、p53乙酰化和B细胞淋巴瘤2相关X蛋白表达降低，随后减弱LPS诱导的凋亡性细胞死亡和自噬。本研究结果表明，[具体物质]多糖激活SIRT1并抑制LPS诱导的ROS产生、凋亡和自噬。这可能对[具体疾病]感染的治疗具有关键意义。
