Ferulic Acid Alleviates Inflammation and Promotes Osteogenic Differentiation in Periodontitis by Inhibiting NF-κB Pathway.

BACKGROUND: Periodontitis refers to a chronic inflammatory illness that induces the destruction of periodontal tissues and can be driven by bacterial lipopolysaccharide (LPS) of pathogens. This study investigated the anti-inflammatory potential and underlying mechanisms of ferulic acid (FA) in periodontitis. METHOD: An in vitro periodontitis model was established by treating human periodontal ligament stem cells (hPDLSCs) with 10 µg/mL LPS for 24 h. The experimental groups included a control group, an LPS-treated group, and an LPS + FA cotreatment group. In addition, phorbol 12-myristate 13-acetate (PMA) treatment was used for nuclear factor κB (NF-κB) pathway activation. Cell proliferation was evaluated using the Cell Counting Kit-8 (CCK-8) test, and osteogenic differentiation was measured by alkaline phosphatase (ALP) and alizarin red S (ARS) staining. Apoptosis was detected with flow cytometry utilizing Annexin V-APC/PI double staining. Protein expressions were measured by Western blot. Inflammatory cytokine secretion was measured via enzyme-linked immunosorbent assay (ELISA) kits. RESULT: This study uncovered that FA alleviates LPS-induced inflammatory responses in hPDLSCs, promoting cell proliferation and osteogenic differentiation. FA inhibits NF-κB pathway activation, reduces proinflammatory cytokines (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-1β, IL-6), increases anti-inflammatory cytokine IL-10, and upregulates osteogenic markers (runt-related transcription factor 2 [Runx2], type I collagen [COL1], osteopontin [OPN], osteocalcin [OCN]). However, the protective effects of FA are reversed by the NF-κB activator PMA, indicating that its therapeutic efficacy primarily depends on NF-κB signaling regulation. CONCLUSION: This study evaluated FA's effects on inflammation and osteogenic function in LPS-induced hPDLSCs, revealing its potential to alleviate periodontitis via NF-κB pathway inhibition and identifying a possible therapeutic target for periodontal disease.