Sevoflurane exerts a more marked influence compared with propofol on gene expression in patients undergoing coronary...

The aim of the present study was to elucidate the influence of the anesthetics propofol and sevoflurane on gene expression in patients undergoing coronary artery bypass graft surgery (CABG) and to provide a basis for the selection of the appropriate anesthetic. The gene expression profiles of patients receiving one of the two anesthetics were analyzed prior to and following the induction of anesthesia. GSE4386 microarray data obtained from the Gene Expression Omnibus database was used to identify the differentially expressed genes (DEGs) by significance analysis of the microarray. The data set contained data regarding atrial tissue samples from 40 patients that underwent CABG, and that received either propofol (n=10) or sevoflurane (n=10) or were control subjects (n=20). The 20 control samples comprised the same patients prior to undergoing CABG. The Kyoto Encyclopedia of Genes and Genomes and Gene Ontology (GO) Enrichment Analysis was applied to the DEGs using the Database for Annotation, Visualization and Integration Discovery functional annotation bioinformatics microarray tool. A total of 242 and 560 DEGs were identified in the human atrial samples treated with propofol and sevoflurane, respectively. Among these, 116 upregulated DEGs and no downregulated DEGs were found to be unique to sevoflurane, while 10 upregulated and 212 downregulated DEGs were unique to propofol. The majority of the pathways that were significantly over-represented among the upregulated DEGs were associated with the immune response, such as Toll- and NOD-like receptors and Jak-STAT signaling pathways. GO enrichment analysis revealed that the downregulated DEGs unique to sevoflurane treatment were involved in the immune response and glucose metabolism, while the upregulated DEGs were associated with cellular ion homeostasis and epithelial cell development. Compared with propofol, sevoflurane appeared to exert a more marked effect on biological pathways, such as drug metabolism, glycolysis, cellular ion homeostasis and epithelial cell development.