Byakangelicin Improves Periodontitis by Inhibiting Inflammation and Promoting Osteogenic Differentiation

This study aimed to investigate the effects of Byakangelicin on the progression of periodontitis. The viability and proliferation of periodontal ligament cells were assessed using Cell Counting Kit-8 and 5-Ethynyl-2'-deoxyuridine assays. The proinflammatory cytokines Tumor Necrosis Factor-alpha, Interleukin-6, and Interleukin-1 beta levels were evaluated through Enzyme-Linked Immunosorbent Assay. Western blotting was employed to assess protein expression levels. Alizarin Red staining was used to examine mineralization capability, while Alkaline Phosphatase activity was determined using a commercial Alkaline Phosphatase kit. In this study, periodontal ligament cells were initially treated with lipopolysaccharide (10 mu g/mL) to establish a periodontitis cell model. It was demonstrated that Byakangelicin inhibited cell proliferation in lipopolysaccharide-stimulated periodontal ligament cells. Additionally, the enhancement of pro-inflammatory factors Tumor Necrosis Factor-alpha, Interleukin-6, and Interleukin-1 beta following lipopolysaccharide exposure was mitigated by Byakangelicin treatment at concentrations of 2.5, 5, and 10 mu mol/L. The impaired osteogenic differentiation caused by lipopolysaccharide was reversed following Byakangelicin treatment. Furthermore, it was discovered that Byakangelicin could alleviate the activation of the nuclear factor kappa-B pathway induced by lipopolysaccharide exposure. Overall, Byakangelicin demonstrated therapeutic potential in periodontitis by inhibiting inflammation and promoting osteogenic differentiation through the nuclear factor kappa-B pathway.