LncRNA-SNHG3 promotes neuroinflammation post-intracerebral hemorrhage by regulating the miR-106b-5p/TXNIP axis

BackgroundIntracerebral hemorrhage (ICH) stands as the most fatal stroke subtype, lacking any specific therapeutic approach yielding benefits for functional recovery.ObjectivesWe aimed to explore the involvement of long non-coding RNA small nucleolar RNA host gene 3 (lncRNA-SNHG3) in post-ICH neuroinflammation, offering a novel rationale for ICH treatment.ResultsBrain tissues of ICH-induced mice exhibited upregulated levels of lncRNA-SNHG3. Inhibition of lncRNA-SNHG3 led to reduced modified neurological severity scores, diminished brain edema, and attenuated inflammatory infiltration, coupled with reduced levels of tumor necrosis factor-alpha/interleukin-1 beta. By repressing miR-106b-5p via targeted binding, lncRNA-SNHG3 facilitated the inhibition of transcriptional and protein levels of thioredoxin-interacting protein (TXNIP) through targeted binding to TXNIP mRNA. The counteraction of miR-106b-5p inhibition or the upregulation of TXNIP reversed the ameliorative effect of sh-SNHG3 on neuroinflammation.ConclusionCompetitive binding of lncRNA-SNHG3 to miR-106b-5p resulted in the upregulation of TXNIP, consequently inducing neuroinflammation and exacerbating ICH-induced damage.