LAUSR

ABSTRACT This study aimed to explore the potential genes and pathways associated with bupivacaine-induced apoptosis. Human neuroblastoma cell line SH-SY5Y was used in this study. The effect of bupivacaine on cell viability of SH-SY5Y was detected by Cell Counting Kit-8. Transcriptome sequencing was performed for SH-SY5Y cells that were treated and untreated with bupivacaine based on the HiSeq 4000 sequencing platform. The sequencing results were analyzed using bioinformatics methods, including differentially expressed genes (DEGs) identification, functional enrichment analysis, protein–protein interaction (PPI) network analysis and module analysis. The cell viability of SH-SY5Y cells decreased significantly after bupivacaine treatment (p < .01). Based on the HiSeq 4000 sequencing platform, we obtained a global overview of the transcriptome of SH-SY5Y treated with/without bupivacaine. Bioinformatics analysis identified 335 up-regulated and 294 down-regulated DEGs in bupivacaine group. They were significantly enriched in cell cycle-associated functions and pathways and cAMP signaling pathway. In the PPI network, proliferating cell nuclear antigen (PCNA), v-Akt murine thymoma viral oncogene homolog 3 (AKT3), cyclin-dependent kinase inhibitor 1A (CDKN1A) and cell division cycle 6 (CDC6) had high topology scores. Module analysis obtained two sub-network modules (cluster 1 and cluster 2). PCNA, CDC6, CDKN1A and AKT3 may play important roles in bupivacaine-induced apoptosis. Additionally, bupivacaine may also induce apoptosis via pathways of cell cycle and cAMP signaling pathway.