Upregulation of miR-215 attenuates propofol-induced apoptosis and oxidative stress in developing neurons by targeting LATS2

• DOI: 10.1186/s10020-020-00170-6
• Publication Date: 2020-05-06T11:03:42Z
• Authors: Fang Tang; Lili Zhao; Qi Yu; Tianyin Liu; Hongyan Gong; Zhiyi Liu; Qing Li
• Keywords: Neurotoxicity; Viability assay; MTT assay

Abstract Background Propofol is an intravenous anesthetic agent that commonly induces significant neuroapoptosis. MicroRNAs (miRNAs) have been reported to participate in the regulation of propofol exposure-mediated neurotoxicity. MiR-215, as one miRNAs, was found regulate nerve cell survival. However, mechanism through which miRNAs neurotoxicity still unclear. Methods Real-time PCR used detect miR-215 expression level. Cell viability measured using MTT assay. apoptosis examined via flow cytometry analysis. ROS, MDA, LDH and SOD levels were assayed ELISA kits. Dual luciferase reporter assay identified interaction between large tumor suppressor 2 (LATS2). Protein level detected western blot Results MiR-215 downregulated propofol-treated rat hippocampal neurons. mimics promoted reduced neonatal neuron. also caused inhibition oxidative stress evidenced by suppression MDA well increase In addition, we (LATS2) a target decreased LATS2 Further, overexpression suppressed effect on propofol-induced Conclusion Taken together, demonstrate attenuates neuron targeting LATS2, suggesting may provide new candidate for treatment exposure-induced