Department of Anesthesiology, Ningbo No.6 Hospital, Ningbo, Zhejiang Province, PR China.
Department of Anesthesiology, Ningbo No.6 Hospital, Ningbo, Zhejiang Province, PR China.
Life Sci. 2020 Jul 15;253:117626. doi: 10.1016/j.lfs.2020.117626. Epub 2020 Apr 1.
Postoperative cognitive dysfunction (POCD) is a common postoperative complication that is associated with increased morbidity and mortality. However, the mechanism of pathogenesis of POCD still remains largely unknown. The aim of the study was to investigate the function and mechanism of lncRNA PCAI in POCD.
Knockdown and overexpression studies were performed to analyze the function of lncRNA PCAI in cultured BV-2 cell lines treated with LPS to mimic the neuroinflammation. Real-time PCR, western blot, ELISA were used to determine the expression level of inflammation markers. Rescue experiment was performed to prove the relationship between PCAI and SUZ12.
We found that the expression of lncRNA PCAI was decreased with the increasing concentrations of LPS. Knockdown of lncRNA PCAI inhibited the cell death rates and attenuated the cell inflammation via ELISA and real-time PCR. Besides, downregulated of lncRNA PCAI can protect the mitochondrial function via membrane potential assay. Overexpression of lncRNA PCAI can promote the cell death and inflammation response induced by LPS. We also provided mechanism study about lncRNA PCAI that negatively regulating SUZ12. Rescue experiment also verified the results.
We performed comprehensive study of functional analysis of lncRNA PCAI in POCD and proved its mechanism, which negatively regulate SUZ12. Our study provided new clues for the clinical intervention and targets for POCD.
术后认知功能障碍（POCD）是一种常见的术后并发症，与发病率和死亡率的增加有关。然而，POCD 的发病机制仍很大程度上未知。本研究旨在探讨长链非编码 RNA PCAI 在 POCD 中的功能和作用机制。
通过敲低和过表达研究来分析 lncRNA PCAI 在 LPS 处理的培养 BV-2 细胞系中模拟神经炎症时的功能。实时 PCR、western blot、ELISA 用于确定炎症标志物的表达水平。进行挽救实验以证明 PCAI 和 SUZ12 之间的关系。
我们发现随着 LPS 浓度的增加，lncRNA PCAI 的表达降低。敲低 lncRNA PCAI 通过 ELISA 和实时 PCR 抑制细胞死亡率并减轻细胞炎症。此外，下调 lncRNA PCAI 可以通过膜电位测定来保护线粒体功能。lncRNA PCAI 的过表达可以促进 LPS 诱导的细胞死亡和炎症反应。我们还提供了关于 lncRNA PCAI 的负调控 SUZ12 的机制研究。挽救实验也验证了这些结果。
我们对 POCD 中 lncRNA PCAI 的功能分析进行了全面研究，并证明了其机制，即负调控 SUZ12。我们的研究为 POCD 的临床干预和靶点提供了新的线索。
