Treatment with Panax notoginseng
saponin (PNS) can prevent neurological damage in
middle cerebral artery occlusion model rats to promote recovery after a
stroke. However, the exact molecular mechanisms are unknown and require further study. In the present study,
mRNA sequencing was employed to investigate differential gene expression between model and
sham groups, and between model and PNS‑treated groups. Enrichment of gene data was performed using Gene Ontology analysis and the Kyoto Encyclopedia of Genes and Genomes database. Hub genes were identified and networks were constructed using Cytoscape that were further verified by reverse transcription‑quantitative PCR. A total of 1,104 genes of interest were found, which included 690 upregulated and 414 downregulated genes that were identified when the model was compared with the
sham group. Additionally, 817 genes of interest, which included 390 upregulated and 427 downregulated genes, were identified when the PNS‑treated group was compared with the model group. There were 303 overlapping genes of interest between the analysis of model to
sham groups, and the analysis of model to PNS‑treated groups. The top 10 genes from the 303 aberrantly expressed genes of interest included
ubiquitin conjugating enzyme E2 variant 2, small ubiquitin‑related modifier 1, small
RNA binding
exonuclease protection factor La, Finkel‑Biskis‑Reilly murine
sarcoma virus (FBR‑MuSV) ubiquitously expressed, centrosomal
protein 290 kDa, DNA‑directed
RNA polymerase II subunit K, cullin‑4B, matrin‑3 and
vascular endothelial growth factor receptor 2. In conclusion, these genes may be important in the underlying mechanism of PNS treatment in
ischemic stroke. Additionally, the present data provided novel insight into the pathogenesis of
ischemic stroke.