LAUSR

Lumbar spinal stenosis is a common orthopedic disease in clinical practice at present. Postoperative cognitive dysfunction (POCD) refers to the phenomenon of impaired memory. However, whether long noncoding RNA (LncRNA) GAS5 contributes to the mechanism of cognitive function in undergoing lumbar spinal canal decompression remains unknown. Thus, the present study investigated the precise details of LncRNA GAS5 involvement in Postoperative cognitive dysfunction of patients undergoing lumbar spinal canal decompression. Patients undergoing lumbar spinal canal decompression with cognitive function and Normal healthy volunteers were obtained. C57BL/6 mice were maintained with a 2% concentration of sevoflurane in 100% oxygen at a flow rate of 2 L minute-1 for 4 hours. LncRNA GAS5 gene expression were up-regulated in patients undergoing lumbar spinal canal decompression. In mice model, LncRNA GAS5 gene expression also increased. LncRNA GAS5 promoted neuroinflammation in vitro model. LncRNA GAS5 raised cognitive impairment and increased neuroinflammation in mice model. LncRNA GAS5 suppressed miR-137 in vitro model. MiR-137 reduced neuroinflammation in vitro model. MiR-137 suppressed TCF4 protein expression in vitro model. Transcription factor TCF4 activates the expression of bHLH. Taking together, this experiment provide the first experimental and clinical evidence that LncRNA GAS5/miR-137 promoted anesthesia-induced cognitive function to increase inflammatory bodies in patients undergoing lumbar spinal canal decompression, suggesting it may be a biomarker of POCD and a potential therapeutic target for POCD.