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Spinal cord injury (SCI) is one of the most severely devastating events that occur in the central nervous system (CNS) and may result in complete or incomplete loss of motor and sensory function 1, 2. SCI is associated with high incidence, disability, and mortality rates; it was reported that the age-standardized incidence rate of SCI was 13 (11-16) per 100,000, and the years of life lived with disability (YLDs) caused by SCI was 9.5 (6.7–12.4) million in 2016 3. High-energy injuries, such as high falls and motor vehicle accidents, were the leading aetiologies of new SCI cases 4. In 2016, SCI-related direct costs were reported to exceed 45 billion United States dollars (USDs) per year in the USA 5, which resulted in a great economic burden for patients, families, and society as a whole. However, there are no curative treatments available in the clinic 6, 7. The complicated mechanisms of SCI include primary and secondary injury. Mechanical traumatic injury causes primary injury, including the disruption of the blood-spinal cord barrier, ischaemia, oedema, compromised vascular supply, and haemorrhage, followed by secondary injury, including inflammatory cell infiltration, proinflammatory cytokine release, and necrotic cell death; these phenomena lead to the apoptosis and necrosis of neurons and glial cells, which may result in the loss of neural circuits and demyelination 8. Secondary injury can be divided into the acute, subacute, moderate, and chronic phases, and the subacute phase of SCI lasts from 2 days to 2 weeks 6. In this phase, oedema, vasospasm, and vessel thrombosis cause further ischaemia. The ongoing infiltration of inflammatory cells leads to the formation of cystic microcavities and more cell death owing to the damaged extracellular architecture of tissues and cells. Moreover, the proliferation of astrocytes is also important in the changes in the microenvironment of this stage postSCI 9. These pathological processes may play crucial roles in the secondary injury of SCI, and this stage may be a potential treatment window. Therefore, it is necessary to further understand the pathological mechanisms that occur after SCI to develop new therapeutic measures to better promote the neurological function of SCI patients. Long noncoding RNAs (lncRNAs), noncoding RNAs with lengths of more than 200 nucleotides, participate in several regulatory processes related to gene expression, including gene transcription and translation modulation, chromatin modification and DNA methylation 10-12. It has been reported that lncRNAs may play a significant role in several CNS degenerative diseases 13. However, there are few studies on the roles of these molecules after SCI. Thus, for this study, microarray analyses were used to investigate the differential expression of mRNAs and lncRNAs one week post SCI in a rat contusion model. Subsequently, functional enrichment analysis of these differential mRNAs was performed. In addition, the interaction between differentially expressed lncRNA(DE lncRNA) and mRNA(DE mRNA) was analyzed by bioinformatics. This study may be helpful for exploring the pathophysiological mechanism underlying SCI and to develop and formulate new therapeutic measures.