SNHG1 alleviates the oxidative stress and inflammatory response in traumatic brain injury through regulating miR-377-3p/DUSP1 axis

ObjectivesTo investigate the role of short nucleolar RNA host gene 1 (SNHG1) in regulating inflammation and brain injury in traumatic brain injury (TBI). MethodsThe Feeney's free-falling method was used to induce moderate TBI model in mice. Lipopolysaccharide (LPS) was employed to construct the microglia in vitro. Reverse transcription-PCR (RT-PCR) was conducted to monitor expression of SNHG1, microRNAs (miR)-377-3p, oxidative and inflammatory factors. TdT-mediated dUTP nick end labeling and immunohistochemistry were adopted to determine neuronal cell apoptosis. Flow cytometry was conducted to measure apoptosis. Moreover, Bax, Bcl2, Caspase3, dual-specific phosphatase-1 (DUSP1)/mitogen-activated protein kinase/NF-KB were tested by western blot. Furthermore, bioinformatics, dual-luciferase assay and RNA-binding protein immunoprecipitation experiment were implemented to verify the targeting relationship among SNHG1, miR-377-3p and DUSP1. ResultsSNHG1 was knocked down, while miR-377-3p was overexpressed in TBI mice and lipopolysaccharide-induced microglia. Meanwhile, overexpressing SNHG1 reduced neuronal damage and weakened the oxidative stress and inflammation in TBI on matter in vivo or in vitro. Additionally, overexpressing SNHG1 attenuated miR-377-3p-mediated inflammatory factors, oxidative stress and neuronal damage. Moreover, miR-377-3p was the target of SNHG1 and DUSP1. ConclusionsThis study provides a better understanding of the SNHG1/miR-377-3p/DUSP1 axis in regulating the development of TBI, which is helpful to formulate a treatment plan for TBI.