Objective: Elderly patients are prone to postherpetic neuralgia (PHN), which may cause anxiety, depression, and sleep disorders and reduce quality of life. As a result, the life quality of patients was seriously reduced. However, the pathogenesis of PHN has not been fully elucidated, and current treatments remain inadequate. Therefore, it is important to explore the molecular mechanism of PHN.
Methods: We analyzed the GSE64345 dataset, which includes gene expression from the ipsilateral dorsal root ganglia (DRG) of PHN model rats. Differentially expressed genes (DEGs) were identified and analyzed by Gene Ontology. Protein-protein interaction (PPI) network was constructed. The miRNA associated with neuropathic pain and inflammation was found in miRNet. Hub genes were identified and analyzed in Comparative Toxicogenomics Database (CTD). miRNA-mRNA networks associated with PHN were constructed.
Results: A total of 116 genes were up-regulated in the DRG of PHN rats, and 135 genes were down-regulated. Functional analysis revealed that variations were predominantly enriched for genes involved in neuroactive ligand-receptor interactions, the Jak-STAT signaling pathway, and calcium channel activity. Eleven and thirty-one miRNAs associated with neuropathic pain and inflammation, respectively, were found. Eight hub genes (S1PR1, OPRM1, PDYN, CXCL3, S1PR5, TBX5, TNNI3, MYL7, PTGDR2, and FBXW2) associated with PHN were identified.
Conclusions: Bioinformatics analysis is a useful tool to explore the mechanism and pathogenesis of PHN. The identified hub genes may participate in the onset and development of PHN and serve as therapeutic targets.
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| http://dx.doi.org/10.1155/2020/1380504 | DOI Listing |
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