Long non‐coding RNA SNHG5 mediates periodontal inflammation through the NF‐κB signalling pathway

Abstract Aim We investigated the role of long non‐coding RNAs and small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of periodontitis. Materials and Methods A ligature‐induced periodontitis mouse model was established, and gingival tissues were collected from patients with periodontitis and healthy controls. Inflammatory cytokines were detected using quantitative reverse transcription‐polymerase chain reaction and western blotting analyses. Direct interactions between SNHG5 and p65 were detected by RNA pull‐down and RNA immunoprecipitation assays. Micro‐computed tomography, haematoxylin and eosin staining, and immunohistochemical staining were used to measure periodontal bone loss. Results SNHG5 expression was down‐regulated in human and mouse periodontal tissues compared to that in the healthy controls. In vitro experiments demonstrated that SNHG5 significantly ameliorated tumour necrosis factor α‐induced inflammation. Mechanistically, SNHG5 directly binds to the nuclear factor‐kappa B (NF‐κB) p65 subunit and inhibits its translocation, thereby suppressing the NF‐κB signalling pathway activation and reducing the nucleotide‐binding oligomerization domain‐like receptor family pyrin domain‐containing three inflammasome expression. Locally injecting si‐SNHG5 aggravated the periodontal destruction. Conclusion This study revealed that SNHG5 mediates periodontal inflammation through the NF‐κB signalling pathway, providing a potential therapeutic target for periodontitis treatment.