Abstract

Introduction and aims Pulpitis represents a prevalent dental condition where inflammatory tissue damage can advance into irreversible stages or pulp death, ultimately compromising oral health-related quality of life. This study investigated the role and underlying mechanisms of long noncoding RNA SATB1-AS1 in pulpitis progression, offering potential therapeutic targets for this condition. Methods This study included 50 patients with irreversible pulpitis (pulpitis group) and 50 age- and gender-matched orthodontic extraction controls (control group). The expression of SATB1-AS1 in pulpitis tissues was assayed using real-time quantitative PCR. A pulpitis model was established by treating human dental pulp stem cells (DPSCs) with lipopolysaccharide (LPS). Evaluation of DPSC proliferation was performed using CCK-8. The levels of cell cycle-related proteins and inflammatory factors were measured by ELISA, and oxidative stress was evaluated by detecting superoxide dismutase, glutathione peroxidase, glutathione, and malondialdehyde. Bioinformatics tools were utilized to identify potential targets, followed by experimental validation through dual-luciferase reporter assays. Results Downregulation of SATB1-AS1 was identified in diseased pulpitis tissues and cell models. In LPS-induced DPSCs, SATB1-AS1 facilitated cell proliferation and modulated Cyclin D1 and p21 expression. Furthermore, SATB1-AS1 alleviated the LPS-induced release of IL-1β, IL-6, and IL-8, and mitigated oxidative stress-related injury by altering the levels of superoxide dismutase, glutathione peroxidase, glutathione, and malondialdehyde. MiR-15a-5p was negatively modulated by SATB1-AS1. Concurrent expression of miR-15a-5p eliminated the beneficial effects of SATB1-AS1 on DPSC function. Further investigation identified E2F3 as a target of miR-15a-5p, establishing the SATB1-AS1/miR-15a-5p/E2F3 axis as a regulatory pathway in LPS-treated DPSCs. Conclusion The findings indicate that SATB1-AS1 potentially miti