Peroxisome proliferator-activated receptor pathway and key genes in cerebellar dysfunction induced by chronic intermittent alcohol exposure: a transcriptomic study.

Abstract

Background: We conducted a transcriptomic analysis to examine cerebellar transcriptional changes in a mouse model of chronic intermittent alcohol exposure.

Methods: We established a mouse model of chronic intermittent alcohol exposure and conducted a cerebellar transcriptomic analysis. After identifying differentially expressed genes, we analyzed pathway enrichment using the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology. We subsequently constructed a protein - protein interaction network and screened for key genes whose expression levels were validated by real-time quantitative reverse transcription polymerase chain reaction.

Results: We identified 212 differentially expressed genes. The peroxisome proliferator-activated receptor (PPAR) pathway was the pathway with the most significant differential expression in the model of chronic intermittent alcohol exposure. Bloc1s6, Gsk3b, Ppard, and Napb were identified as key target genes. The PPAR pathway and these four target genes may be involved in the mechanisms underlying cerebellar dysfunction induced by chronic alcohol exposure and may also contribute to the development of increased alcohol preference.

Conclusion: The PPAR pathway and four target genes (Bloc1s6, Gsk3b, Ppard, and Napb) may contribute to cerebellar dysfunction and increased alcohol preference induced by chronic alcohol exposure. These findings could help identify potential therapeutic targets for chronic alcohol exposure and alcohol preference and support further investigation into the underlying mechanisms involved.