Abstract
Aim
We investigated the role of the long non-coding RNA (lncRNA), 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 from patients with periodontitis and healthy controls were collected. Inflammatory cytokines were detected using qRT-PCR and western blotting analyses. Direct interactions between SNHG5 and p65 were detected by RNA pull-down and RNA immunoprecipitation assays. Micro-computed tomography, hematoxylin and eosin staining, and immunohistochemical staining were used to measure periodontal bone loss.
Results
SNHG5 expression was downregulated in human and mouse periodontal tissues compared to that in the healthy controls. In vitro experiments demonstrated that SNHG5 significantly ameliorated tumor necrosis factor-α (TNFα)-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 signaling pathway activation and reducing the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 inflammasome expression. Locally injecting si-SNHG5 aggravated the periodontal destruction.
Conclusion
This study revealed that SNHG5 mediates periodontal inflammation through the NF-κB signaling pathway, providing a potential therapeutic target for periodontitis treatment.
This article is protected by copyright. All rights reserved.
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου