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.

中文翻译：

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长的非编码RNA SNHG16通过上调microRNA-423-5p减少PC-12细胞中过氧化氢诱导的细胞损伤。

长非编码RNA（lncRNA）的功能已在脊髓损伤（SCI）中得到了广泛探索。但是，lncRNA-小核仁RNA宿主基因16（lncRNA-SNHG16）的影响在SCI中仍未得到很好的记录。该研究探索了SNHG16对H2O2损伤的PC-12细胞的影响。将PC-12细胞与H2O2处理，检测细胞活力，凋亡，自噬和ROS水平。进行RT-qPCR探索SNHG16或miR-423-5p在H2O2刺激的细胞中的表达。用pc-SNHG16或miR-423-5p抑制剂转染后，研究了SNHG16和miR-423-5p在H2O2损伤的细胞中的功能。AMPK和ERK1 / 2途径最终通过Western blot评估。我们发现H2O2在PC-12细胞中引起细胞损伤，并且在H2O2处理的细胞中观察到SNHG16的抑制。如抑制细胞凋亡，自噬和ROS水平所表明的，过表达的SNHG16显着减轻了H2O2诱导的细胞损伤。此外，SNGH16增强了miR-423-5p的表达，并且miR-423-5p的抑制作用取消了SNGH16对H2O2损伤的PC-12细胞的保护作用。SNGH16通过上调H2O2损伤的PC-12细胞中的miR-423-5p介导AMPK和ERK1 / 2途径。总之，这些发现表明，SNGH16通过介导PC-12细胞中的miR-423-5p减轻了H2O2引起的细胞损伤。这些发现可能揭示了SNHG16对SCI的影响，这为补救SCI提供了新的参考。H2O2引起PC-12细胞的细胞损伤；SNHG16减轻H12O2诱导的PC-12细胞损伤。SNGH16增强H2O2刺激的PC-12细胞中miR-423-5p的表达；MiR-423-5p抑制取消了SNGH16对PC-12细胞的保护作用；SNGH16通过上调miR-423-5p介导AMPK和ERK1 / 2途径。