lncRNA SNHG6 regulates neuroinflammation in traumatic brain injury by inhibiting the expression of miR-101-3p

Abstract Objectives This study was to investigate the altered expression of SNHG6 in individuals suffering from traumatic brain injury (TBI), as well as the correlation between varying degrees of injury severity and patient’s prognosis, and to explore the impact of SNHG6 on oxygen-glucose deprivation (OGD)-induced cell damage. Methods A cohort of 121 patients with TBI were included in this study, including 71 mild patients and 50 severe patients. Reverse Transcription-Polymerase Chain Reaction (RT-qPCR) was used to determine the levels of SNHG6 and miR-101–3p. Receiver Operating Characteristic (ROC) curves were used to analyze the role of SNHG6 in distinguishing TBI patients with different degrees and TBI patients with different prognosis. The cell model was constructed by OGD damage, the cell proliferation capacity was detected by Cell Counting Kit-8 (CCK-8) assay, and the concentrations of inflammatory factors in the cells were detected by ELISA kit. Results Patients with severe TBI had higher levels of SNHG6 expression than those with mild TBI. And the expression of SNHG6 in patients with poor prognosis was higher than that in patients with good prognosis. SNHG6 could distinguish severe TBI patients from those mild TBI patients and predict the prognosis of patients with TBI. SNHG6 regulated cell proliferation and inflammation after OGD injury by inhibiting the expression of miR-101–3p. Conclusions SNHG6 may be a biomarker for TBI, SNHG6 may affect TBI by regulating the expression of miR-101–3p.