Background
Propofol, an intravenous sedative-hypnotic agent, is demonstrated to have antioxidant properties. The
Conclusion
Propofol inhibited oxidative stress and inflammation in MPP+-induced neuroblastoma cells by targeting the HOTAIRM1/miR-519a-3p axis, implying the potential protective function of propofol against oxidative damage.
Methods
The proliferation and apoptosis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT), EdU, and flow cytometry assays, respectively. The protein expression level was quantified by western blot assay. Inflammation and oxidative stress were determined by measuring the release of inflammatory factors, along with intracellular reactive oxygen species (ROS), lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. The real-time quantitative polymerase chain reaction (RT-qPCR) was conducted to assess the expression levels of HOXA transcript antisense RNA, myeloid-specific 1 (HOTAIRM1), and miR-519a-3p in cells. The interaction relationship between HOTAIRM1 and miR-519a-3p was confirmed by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays.
Results
Treatment with MPP+ has been observed to induce apoptosis, oxidative stress, and inflammation in neuroblastoma cells, which were abolished by propofol or silencing of HOTAIRM1. Importantly, the increase of HOTAIRM1 and the decrease of miR-519a-3p caused by MPP+ were reversed by propofol in neuroblastoma cells. In addition, miR-519a-3p was a target of HOTAIRM1, and inhibition of miR-519a-3p abolished HOTAIRM1 silencing-induced effects on neuroblastoma cells. Moreover, functional experiments revealed that propofol might weaken MPP+-induced apoptosis, oxidative stress, and inflammation by regulating the HOTAIRM1/miR-519a-3p axis.