Conclusions
miR-25 protects PC-12 cells against H2O2-induced oxidative damage though regulation of Nrf2 and activation of Wnt/β-catenin and PI3 K/AKT/ERK signaling.
Methods
SCI model was established in C57BL/6 mice, then miR-expression in the injured spinal cords were detected by qRT-PCR. PC-12 cells were exposed to H2O2 conditions to establish an in vitro model of SCI. PC-12 cells were transfected with expressing vector or antisense oligonucleotides (ASO) of miR-25. The effects of miR-25 expression on H2O2-induced oxidative damage was evaluated by detection of cell viability, apoptosis, ROS activity, HIF-α and γH2A expression, and the level of inflammatory mediators. The expression of Nrf2 in cells was silenced by transfection with Nrf2 siRNA, and the effects of Nrf2 silence on miR-25-mediated PC-12 cells were detected. Besides, the expression of main proteins in Wnt/β-catenin and PI3 K/AKT/ERK signaling were assessed.
Objective
Spinal cord injury (SCI) is associated with modulation of different microRNAs (miRs). This study aims to explore the role of miR-25 in PC-12 cells to reveal the potential of miR-25 in SCI treatment.
Results
miR-25 was low expressed in injured spinal cords. miR-25 protected PC-12 cells against H2O2-induced oxidative damage, as evidenced by significant suppression in cell apoptosis, increase in cell viability, decrease in the level of ROS, HIF-α and γH2A, and decrease in inflammatory mediators (IL-1β, TNF-α, IL-6, and MCP-1). However, Nrf2 silence abolished the protective functions of miR-25 on H2O2-induced damage. Furthermore, we found that Wnt/β-catenin and PI3 K/AKT/ERK signaling were activated by miR-25. Conclusions: miR-25 protects PC-12 cells against H2O2-induced oxidative damage though regulation of Nrf2 and activation of Wnt/β-catenin and PI3 K/AKT/ERK signaling.