Therapeutic Potential of Synthetic Human β-Defensin 1 Short Motif Pep-B on Lipopolysaccharide-Stimulated Human Dental Pulp Stem Cells

• Published in: Mediators of inflammation 2022-01, Vol.2022, p.6141967-12
• Main Authors: Shi, Jue, Hu, Zihe, Zhou, Yanyan, Zuo, Minghao, Wu, Haiyan, Jin, Wenjing, Xie, Zhijian
• Format: Article
• Language: English
• Subjects: Alkaline phosphatase; Anti-inflammatory agents; beta-Defensins - metabolism; Cell Differentiation; Cell Proliferation; Cells, Cultured; Chemotaxis; Cholecystokinin; Dental caries; Dental Pulp; Experiments; Flow cytometry; Gene expression; Health aspects; Humans; Immunoregulation; Inflammation; Intracellular signalling; L-Lactate dehydrogenase; Lactic acid; Lipopolysaccharides; Lipopolysaccharides - metabolism; Lipopolysaccharides - pharmacology; MAP kinase; Mineralization; NF-κB protein; Peptides; Phosphatases; Proteins; Signal transduction; Stem Cells; Trauma
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1155/2022/6141967

Dental pulp inflammation is a widespread public problem usually caused by caries or trauma. Alleviating inflammation is critical to inflamed pulp repair. Human β-defensin 1 short motif Pep-B is a cationic peptide that has anti-inflammatory, antibacterial, and immunoregulation properties, but its repair effect on human dental pulp stem cells (hDPSCs) under inflammation remains unclear. In this study, we aimed to investigate anti-inflammatory function of Pep-B and explore its therapeutic potential in lipopolysaccharide-(LPS-) induced hDPSCs. CCK-8 assay and transwell assay evaluated effects of Pep-B on hDPSC proliferation and chemotaxis. Inflammatory response in hDPSCs was induced by LPS; after Pep-B application, lactate dehydrogenase release, intracellular ROS, inflammatory factor genes expression and possible signaling pathway were measured. Then, osteo-/odontoblast differentiation effect of Pep-B on LPS-induced hDPSCs was detected. The results showed that Pep-B promoted hDPSC proliferation and reduced LPS-induced proinflammatory marker expression, and western blot result indicated that Pep-B inhibited inflammatory activation mediated by NF-κB and MAPK pathways. Pep-B also enhanced the expression of the osteo-/odontogenic genes and proteins, alkaline phosphatase activity, and nodule mineralization in LPS-stimulated hDPSCs. These findings indicate that Pep-B has anti-inflammatory activity and promote osteo-/odontoblastic differentiation in LPS-induced inflammatory environment and may have a potential role of hDPSCs for repair and regeneration.