Bioinformatics Analysis and Experimental Validation of Two Blood Stasis Patterns in Ischemic Stroke
Objective To explore the differential expression genes(DEGs)and related signaling pathways of the Qi deficiency and blood stasis(QDBS)and Yin deficiency and blood stasis(YDBS)syndromes in ischemic stroke(IS)at the molecular level,elucidating the potential mechanisms and biological basis of blood stasis syndrome in IS.Methods The mRNA expression profile dataset GSE100235 of the two syndromes of IS rats was downloaded from the GEO database,and the limma package of R language was used to screen DEGs.Subsequently,GO and KEGG analyses were performed using the DAVID database.The miRDB and miRWalk databases were used to predict the miRNAs of DEGs,and aa miRNA-mRNA regulatory network was constructed.A protein-protein interaction network was built using the STRING database,and the cytoHubba plug-in was utilized to identify the core target genes.The rat model of QDBS in IS was established by exhaustive swimming training combined with modified Longa's thread embolism,and the rat model of YDBS in IS was established by hydrocortisone injection and thread embolism.RT-qPCR was employed to validate the expression levels of core target genes in rat brain tissues of the two groups.Results A total of 47 DEGs were identified.These genes were mainly involved in biological processes such as neuronal apoptosis,inflammatory response,and adaptive immune response,as well as pathways related to lipid metabolism,atherosclerosis,and C-type lectin receptor signaling.The miRNA-mRNA interaction network consisted of 64 nodes and 55 edges.Five core target genes were obtained,including Ccl2,Selp,Timp1,Ccr1l1,and Fpr1.Conclusion There are significantly differentially expressed genes in QDBS and YDBS syndrome of IS rats.These genes are involved in a variety of biological processes and pathways,and are most closely related to lipid metabolism and atherosclerosis signaling pathways.
Ischemic strokeGEO databaseBioinformatic analysisQi deficiency and blood stasisYin-deficiency blood-stasis
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