Abstract
The present study investigated the role and molecular mechanism of long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript (MALAT)1 in neuropathic pain in rat chronic constriction injury (CCI) model. Reverse transcription-quantitative PCR and western blot analysis were used to detect the expression levels of MALAT1, microRNA (miR)-154-5p and aquaporin (AQP)9 in spinal cord tissue and microglia of CCI rats. ELISA and pain behavioral assays were used to observe the effect of MALAT1 on neuropathic pain and neuroinflammation in model rats, and to verify its molecular mechanism through bioinformatics and luciferase experiments. The results of the present study identified that the expression levels of MALAT1 and AQP9 were upregulated, while miR-154-5p was downregulated in spinal cord tissue and microglia of CCI rats. MALAT1 knockdown in CCI model rats significantly induced the occurrence of neuropathic pain, while the upregulation of miR-154-5p could reverse this process. The present study also identified that miR-154-5p was the target gene of MALAT1, and AQP9 was the target gene of miR-154-5p. AQP9 knockdown promoted the occurrence of neuropathic pain. In conclusion, lncRNA MALAT1 promotes the progression of neuropathic pain in rats by reducing miR-154-5p and increasing AQP9. The MALAT1/miR-154-5p/AQP9 axis can be used as a new therapeutic target for neuropathic pain.
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