Exploring the mechanism of transcutaneous auricular vagus nerve stimulation on improving post-stroke cognitive impairment in MCAO rats using RNA-seq
Our previous findings have shown that taVNS is effective in improving PSCI. However, its specific mechanism and the target genes, biological processes, and signaling pathways it regulates are still unclear and require more in-depth research.  We established a cognitive impairment model in MCAO rats and administered taVNS treatment. Cognitive function was assessed using Y-maze and novel object recognition (NOR) experiments. Pathological changes in hippocampal tissue were observed through HE and Nissl staining. RNA-seq was conducted on hippocampal tissue from each group, and differentially expressed genes (DEGs) were performed for GO and KEGG enrichment. Hub genes were identified using the STRING database and betweenness centrality values. taVNS treatment significantly improved cognitive function (Y-maze and NOR) and pathological morphology of hippocampal tissue (HE and Nissl staining) in the PSCI model rats. A total of 341 taVNS targeted DEGs were identified, and they may be implicated in chromosome segregation, mitotic nuclear division, cell cycle, NOD-like receptor signaling pathway, NF-kappa B signaling pathway, and Toll-like receptor signaling pathway, etc. The expression trends of TLR4, Myd88, and NF-?B mRNAs in the Hub genes were significantly inhibited by taVNS. Overall design: We established a cognitive impairment model in MCAO rats and administered taVNS treatment. Cognitive function was assessed using Y-maze and novel object recognition (NOR) experiments. Pathological changes in hippocampal tissue were observed through HE and Nissl staining. RNA-seq was conducted on hippocampal tissue from each group, and differentially expressed genes (DEGs) were performed for GO and KEGG enrichment. Hub genes were identified using the STRING database and betweenness centrality values.