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Updated: Jul 15, 2026

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse
Published on: July 25, 2011
Construction of Molecular Pathway Network for Cerebral Ischemia and Reperfusion and Screening of Potential Targeted
Qiming Liu1,2, Ye Tian3, Rui Shi1,2
1Graduate School of Hebei University of Chinese Medicine, Shijiazhuang City, Hebei Province, China.
Objective:
To elucidate the molecular mechanisms underlying ischemia-reperfusion (I/R) injury and explore novel therapeutic targets.
Methods:
Raw counts from control, middle cerebral artery occlusion (MCAO), and MCAO+drug groups were processed via the Differential Expression analysis for Sequence data, version 2 (DESeq2) pipeline. Significant differentially expressed genes (DEGs) were identified under thresholds of padj<0.05 and |log2FoldChange|≥1. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, were conducted using clusterProfiler. A protein-protein interaction (PPI) network of the DEGs was then constructed through Search Tool for Retrieval of Interacting Genes/Proteins (STRING) and visualized in Cytoscape, where Hub genes were screened using CytoHubba. Finally, Hub genes were mapped to the Drug-Gene Interaction Database (DGIdb) to identify potential druggable targets.
Results:
A total of 948 upregulated and 419 downregulated DEGs were identified when comparing the MCAO group against controls, while 348 upregulated and 593 downregulated DEGs emerged from the MCAO+drug vs. MCAO comparison. GO and KEGG enrichment analyses indicated that inflammation, immune response, cell cycle, and apoptosis pathways were significantly affected. The PPI network highlighted Cyclin-Dependent Kinase 1 (CDK1), Aurora Kinase B (AURKB), Baculoviral IAP Repeat Containing 5 (BIRC5), and other cell cycle regulators as key Hub genes. DGIdb queries revealed multiple existing inhibitors targeting these Hub genes, suggesting potential therapeutic agents for mitigating cerebral I/R injury.
Conclusion:
Our results provide a comprehensive molecular view of cerebral ischemia-reperfusion damage, pinpointing pivotal genes and pathways involved in inflammation and cell cycle regulation. These findings could aid in developing targeted therapies and offer new insights into stroke management. Further experimental and clinical studies are warranted to confirm the efficacy and safety of these potential interventions.

