Abstract: Te exact mechanisms associated with secondary brain damage following traumatic brain injury (TBI) remain unclear; therefore, identify- ing the critical molecular mechanisms involved in TBI is essential. Te mRNA expression microarray GSE2871 was downloaded from the Gene Expression Omnibus (GEO) repository. GSE2871 comprises a total of 31 cerebral cortex samples, including two post-TBI time points. Te microarray features eight control and seven TBI samples, from 4 hours post-TBI, and eight control and eight TBI samples from 24 hours post-TBI. In this bioinformatics-based study, 109 and 66 diferentially expressed genes (DEGs) were identifed in a Sprague-Dawley (SD) rat TBI model, 4 and 24 hours post-TBI, respectively. Functional enrichment analysis showed that the identifed DEGs were signif- cantly enriched in several terms, such as positive regulation of nuclear factor-κB transcription factor activity, mitogen-activated protein kinase signaling pathway, negative regulation of apoptotic process, and tumor necrosis factor signaling pathway. Moreover, the hub genes with high connectivity degrees were primarily related to infammatory mediators. To validate the top fve hub genes, a rat model of TBI was established using the weight-drop method, and real-time quantitative polymerase chain reaction analysis of the cerebral cortex was per- formed. Te results showed that compared with control rats, Tnf-α, c-Myc, Spp1, Cxcl10, Ptprc, Egf, Mmp9, and Lcn2 were upregulated, and Fn1 was downregulated in TBI rats. Among these hub genes, Fn1, c-Myc, and Ptprc may represent novel biomarkers or therapeutic targets for TBI. Tese identifed pathways and key genes may provide insights into the molecular mechanisms of TBI and provide potential treat- ment targets for patients with TBI. Tis study was approved by the Experimental Animal Ethics Committee of the First Afliated Hospital of Nanchang University, China (approval No. 003) in January 2016.

Key words: bioinformatics, DEGs, diferentially expressed genes, Gene Ontology, hub genes, infammation, Kyoto Encyclopedia of Genes and Genomes, molecular mechanism, traumatic brain injury