No abstract

Novel thiazolidinedione analogues as 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors were synthesized. Compounds 2, 3, and 4 exhibited IC(50) of 25, 8, and 19 nM, respectively. They also significantly increased levels of PGE(2) in A549 cells. To assess the influence of 15-PGDH inhibitor on cochlear blood flow (CBF), 2 was applied intravenously to guinea pigs. It increased their CBFs. Scratch wounds were also analyzed in confluent monolayers of HaCaT cells. Cells exposed to 4 showed significantly improved wound healing with respect to a control.

Heat shock protein-27 (HSP27) is a member of the small HSP family which has been linked to the nuclear factor-kappa B (NF-κB) signaling pathway regulating inflammatory responses. Clinical reports have suggested that low-level light therapy/laser irradiation (LLLT) could be an effective alternative treatment to relieve inflammation during bacterial infection associated with periodontal disease. However, it remains unclear how light irradiation can modulate the NF-κB signaling pathway. We examined whether or not 635 nm irradiation could lead to a modulation of the NF-kB signaling pathway in HSP27-silenced cells and analyzed the functional cross-talk between these factors in NF-κB activation. The results showed that 635 nm irradiation led to a decrease in the HSP27 phosphorylation, reactive oxygen species (ROS) generation, I-κB kinase (IKK)/inhibitor of κB (IκB)/NF-κB phosphorylation, NF-κB p65 translocation and a subsequent decrease in the COX-1/2 expression and prostaglandin (PGE(2) ) release in lipopolysaccharide(LPS)-induced human gingival fibroblast cells (hGFs). However, in HSP27-silenced hGFs, no obvious changes were observed in ROS generation, IKK/IκB/NF-κB phosphorylation, NF-κB p65 translocation, nor in COX-1/2 expression, or PGE(2) release. This could be a mechanism by which 635 nm irradiation modulates LPS-induced NF-κB signaling pathway via HSP27 in inflammation. Thus, HSP27 may play a role in regulating the anti-inflammatory response of LLLT.

Aim This study aims to evaluate the association of salivary S100A8 and A9 proteins with periodontitis and its screening ability for periodontitis cross‐sectionally. Material and Methods We selected 326 participants from the Yangpyeong Cohort: 218 participants with periodontitis and 108 participants without periodontitis. Stage II‐IV periodontitis according to the modification of new international classification of periodontitis was considered as periodontitis. S100A8 and A9 were assayed using enzyme‐linked immunosorbent assay kit. Age, sex, education, smoking, drinking, exercise, and metabolic syndrome were factored as confounders. Analyses of covariance and logistic regression analysis were applied to evaluate the association of S100A8 and A9 with periodontitis. Receiver operating characteristic curve was applied for screening ability. Results Those with periodontitis compared to those without periodontitis showed higher adjusted amount of S100A8 (3694 versus 6757 ng/ml, p < 0.001), but less adjusted amount of S100A9 (1341 versus 1030 ng/ml, p = 0.015). The screening ability of S100A8 and A9 on periodontitis was c‐statistics of 0.69 (p < 0.001) for both S100A8 and A9, 0.67 for S100A8 and 0.63 (p < 0.001) for S100A9. Conclusions Overall, salivary S100A8 and S100A9 could be practical markers for periodontitis. Its screening ability for periodontitis could be beneficial in clinics and at home.

Photodynamic therapy (PDT) of cells is a new treatment modality involving selective delivery of a photosensitive dye into target cells, followed by visible light irradiation. PDT induces cell death by excessive ROS generation. The effects of multiple photosensitizers were owing to the difference in cell types involving sensitizer-specific protein changes linked to resistance. HSP27 is regulated in response to stress and is associated with apoptotic process. The effects of HSP27 on PDT resistance are controversial and unclear. The purpose of this study was to investigate the role of HSP27 down-regulation in the PDT-induced cells and HSP27 regulation in the resistance to PDT. KB cells transfected with HSP27 siRNA were exposed to hematoporphyrin (HP) followed by irradiation at 635 nm at an energy density of 4.5 mW/cm(2). After irradiation, the effects on HSP27 down-regulation were assessed by MTT assay, flow cytometry, confocal analysis, Western blotting and caspase activity. The results of this study showed that down-regulation of HSP27 restored cell survival in HP-PDT-induced apoptotic KB cells. HSP27 down-regulation attenuated PDT-induced apoptosis through caspase-mediated pathway in KB cells. Also, HSP27 silencing regulated Bax, Bcl-2, and PARP protein expression in PDT-induced cells. Therefore, HSP27 down-regulation confers resistance to PDT through interruption of apoptotic protein activity in PDT-induced cell death. HSP27 might contribute to regulating PDT-induced apoptosis in PDT-resistant cells.