Human β- defensin-2 (hBD-2) is an antimicrobial peptide which is produced by epithelial cells after stimulation with microorganisms or inflammatory mediators. However, little is known as to whether the LPS and nicotine induces the expression of hBD-2 in periodontal l igament (PDL) cells. T he p urpose o f this s tudy was t o investigate t he r oles o f MAPKs pathway o f nicotine a nd L PS-induced hBD-2 expression in PDL cells. The maximal expression of hBD-2 was observed in nicotine 5 mM and LPS 1 μg/ml treated PDL cells. Nicotine and LPS induced the phosphorylation of p38, c-Jun N-terminal kinase 1 and 2 (JNK1/2), and extracellular signal-regulated kinases 1 and 2 (ERK1/2) MAPK. ERK1/2 inhibitor SB203580, p38 inhibitor PD98059, and JNK inhibitor SP600125, blocked the effects of nicotine and LPS on hBD-2 upregulation in PDL cells. These results collectively suggest that hBD-2 is up-regulated in nicotine and LPS-treated PDL cells through activation of p38, ERK and JNK MAPKs pathway. Our data regarding the up-regulation of hBD-2 may help us to understand the antimicrobial mechanism in periodontal disease

The present study aimed to verify the effects of DFO on PDL cells, with particular emphasis on focusing on osteoblastic differentiation. Its mechanisms related to heme oxygenase-1 (HO-1) pathway were also analyzed. DFO increased the expression of HO-1 and early osteoblastic differentiation markers, such as alkaline phosphatase (ALP) and bone sialoprotein (BSP). DFO upregulated heme oxygenase-1. Treatment with HO-1 siRNA blocked the DFO-stimulated osteoblastic differentiation and HO-1 expression. The NF-kB inhibitor pyrrolidine dithiocarbamate, phosphatidylinositol 3-kinase inhibitor Wortmannin, and p38 MAPK inhibitor U0126 blocked the effects of DFO on HO-1 expression and osteoblastic differentiation in PDL cells. Collectively, these data suggest that DFO promotes osteoblastic differentiation and induces the expression of defense protein HO-1 probably via PI3K, p38 MAPK, and NF-kB signalling pathways in PDL cells.