Interference of Interleukin-1? Mediated by Lentivirus Promotes Functional Recovery of Spinal Cord Contusion Injury in Rats via the PI3K/AKT1 Signaling Pathway

Purpose. Inflammation and apoptosis after spinal cord contusion (SCC) are important causes of irreversible injury. Interleukin-1? (IL-1?) is a key inflammatory factor that promotes the aggravation contusion. However, specific role regulatory mechanism IL-1? in still unclear. Therefore, this study applied bioinformatics to analyze mine potential gene targets interlinked with IL-1?, animal experiments lentiviral interference technology were used explore whether affected recovery motor function by interfering PI3K/AKT1 signaling pathway. Method. This screen related IL-1?. The rat SCC model was established Allen method, Basso Beattie Bresnahan (BBB) score evaluate cord-injured rats. Immunohistochemistry immunofluorescence localize expression AKT1 proteins tissue. Quantitative polymerase chain reaction Western blot detect protein expressions PI3K, AKT1. RNAi construct lentivirus inhibit investigate effect on relationship among AKT1, downstream pathways. Results. Bioinformatics analysis suggested close between Animal have confirmed closely functional Firstly, from phenomenological level, BBB decreased SCC, located cytoplasm neurons anterior horn cord, levels experimental group higher than those sham operation group. At same time, decreased, results increase Secondly, inhibiting lentivirus-mediated significantly increased, improved. Thirdly, mechanistic revealed In addition, experiment further verified pathway, inhibition upregulated expression, but PI3K unchanged. Conclusion. Inhibition injury rats through upregulation may affect regeneration pathway regulate FOXO, mTOR, GSK3 pathways; thereby hindering It provided new perspective for clinical treatment future.