Abstract
Functions of long non-coding RNAs (lncRNAs) have been widely probed in spinal cord injury (SCI). But, the influences of lncRNA-small nucleolar RNA host gene 16 (lncRNA-SNHG16) is still not well documented in SCI. The study explored the impacts of SNHG16 on H2O2-injured PC-12 cells. PC-12 cells were disposed with H2O2, cell viability, apoptosis, autophagy and ROS level were detected. RT-qPCR was executed to explore SNHG16 or miR-423-5p expression in H2O2-stimulated cells. After transfection with pc-SNHG16 or miR-423-5p inhibitor, the functions of SNHG16 and miR-423-5p in H2O2-injured cells were studied. AMPK and ERK1/2 pathways were finally assessed by western blot. We found that H2O2 evoked cell injury in PC-12 cells, and repressed SNHG16 was observed in H2O2-disposed cells. Overexpressed SNHG16 prominently alleviated H2O2-induced cell injury as indicated by repressing cell apoptosis, autophagy and ROS level. Additionally, SNGH16 enhanced miR-423-5p expression, and miR-423-5p inhibition abrogated the protective effect of SNGH16 on H2O2-injured PC-12 cells. SNGH16 mediated AMPK and ERK1/2 pathways via up-regulating miR-423-5p in H2O2-injured PC-12 cells. In conclusion, these findings indicated that SNGH16 reduced H2O2-evoked cell injury by mediating miR-423-5p in PC-12 cells. The findings might uncover the effect of SNHG16 on SCI, which provide a new reference for remedying SCI. Highlights H2O2 evokes cell injury in PC-12 cells; SNHG16 reduces H2O2-induced cell injury in PC-12 cells; SNGH16 enhances miR-423-5p expression in H2O2-stimulated PC-12 cells; MiR-423-5p inhibition abrogates the protective effect of SNGH16 in PC-12 cells; SNGH16 mediates AMPK and ERK1/2 pathways by up-regulating miR-423-5p.