Ferulic Acid Alleviates Inflammation and Promotes Osteogenic Differentiation in Periodontitis by Inhibiting NF‐ κ B 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 κ B (NF‐ κ B) 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‐ κ B pathway activation, reduces proinflammatory cytokines (tumor necrosis factor‐alpha [TNF‐ α ], interleukin [IL]‐1 β , 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‐ κ B activator PMA, indicating that its therapeutic efficacy primarily depends on NF‐ κ B 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‐ κ B pathway inhibition and identifying a possible therapeutic target for periodontal disease.