An Integrative Bioinformatics Analysis of the Potential Mechanisms Involved in Propofol Affecting Hippocampal Neuronal Cells.

The aim of this study is to probe the possible molecular mechanisms underlying the effects of propofol on HT22 cells. HT22 cells treated with different concentrations were sequenced, and then the results of the sequencing were analyzed for dynamic trends. Expression pattern clustering analysis was performed to demonstrate the expression of genes in the significant trend modules in each group of samples. We first chose the genes related to the trend module for WGCNA analysis, then constructed the PPI network of module genes related to propofol treatment group, and screened the key genes. Finally, GSEA analysis was performed on the key genes. Overall, 2,506 genes showed a decreasing trend with increasing propofol concentration, and 1,871 genes showed an increasing trend with increasing propofol concentration. WGCNA analysis showed that among them, turquoise panel genes were negatively correlated with propofol treatment, and genes with Cor R >0.9 in the turquoise panel were selected for PPI network construction. The MCC algorithm screened a total of five key genes (CD86, IL10RA, PTPRC, SPI1, and ITGAM). GSEA analysis showed that CD86, IL10RA, PTPRC, SPI1, and ITGAM are involved in the PRION_DISEASES pathway. Our study showed that propofol sedation can affect mRNA expression in the hippocampus, providing new ideas to identify treatment of nerve injury induced by propofol anesthesia.