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

Background Intracerebral hemorrhage (ICH) stands as the most fatal stroke subtype, lacking any specific therapeutic approach yielding benefits for functional recovery. Objectives We 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. Results Brain 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-α/interleukin-1β. 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. Conclusion Competitive binding of lncRNA-SNHG3 to miR-106b-5p resulted in the upregulation of TXNIP, consequently inducing neuroinflammation and exacerbating ICH-induced damage.