Krüppel-like factor 5 -mediated Sirtuin6 promotes osteogenic differentiation and inhibits inflammatory injury of lipopolysaccharide-induced periodontal membrane stem cells by inhibiting nuclear factor kappa-B pathway.

Periodontitis is a chronic infectious disease that causes inflammation and immune response and has an ultimate impact on the health of the whole body. Sirtuin6 (SIRT6) and Krüppel-like factor 5 (KLF5) have been reported to regulate the inflammatory response and play an important role in the development of periodontitis. LPS was adopted to induce periodontal ligament stem cells (PDLSCs) to construct a periodontitis cell model. SIRT6 expression was assayed through RT-qPCR and Western blot. Subsequently, after SIRT6 was overexpressed, CCK8 was to appraise cell viability. ELISA analysis was used to estimate inflammatory response. ALP staining, ARS staining, and Western blot were used to detect osteogenic differentiation. The JASPAR website then predicts the binding of transcription factor KLF5 to SIRT6 promoter. The interaction between KLF5 and SIRT6 was verified by a luciferase reporter and ChIP assays. Additionally, the osteogenic differentiation and inflammation in LPS-induced PDLSCs transfected with Ov-SIRT6 and si-KIF5 were also explored. Finally, the protein levels of the nuclear factor kappa-B (NF-κB) pathway-related factors were detected by Western blot to further explore the mechanism. There was a marked decrease in SIRT6 expression in LPS-induced PDLSCs. SITR6 overexpression prevented LPS-induced cell viability loss and inflammation, while promoting osteogenic differentiation. In addition, KLF5 could transcriptionally activate SIRT6. Further, KLF5 knockdown reversed the impacts of SIRT6 on the proliferation, inflammation, and osteogenic differentiation of LPS-induced PDLSCs via mediating NF-κB pathway. Overall, KLF5-mediated SIRT6 promoted the viability and osteogenic differentiation, while inhibiting the inflammatory response of LPS-induced PDLSCs by inhibiting NF-κB pathway.

Increased risk of periodontitis occurrence in patients with rheumatoid arthritis and its association with the levels of IL-1ß and TNF-α in gingival crevicular fluid.

BACKGROUND: Periodontitis (PD) is a chronic inflammatory disease caused by infection of the periodontal supporting tissues. Clinical studies have reported that rheumatoid arthritis (RA) patients have a higher prevalence of PD. This study aimed to explore the correlation between RA and PD. METHODS: A total of 307 RA patients (RA group) and 324 healthy individuals (control group) who received physical examinations during the same period were recruited to this study. The incidence of PD in the two groups was analyzed, and the periodontal disease index (PDI) and bleeding on probing (BOP) were recorded. Then, 42 RA patients with PD and 56 control group patients with PD were selected for further analysis. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin 1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in the gingival crevicular fluid (GCF) of the two groups. For patients with both RA and PD, the level of serum C-reactive protein (CRP) and the duration of morning stiffness were also recorded. RESULTS: The prevalence of PD in the RA group (51.5%) was significantly higher than that in the control group (31.2%), and the prevalence of PD also increased notably with the increase of age and the duration of the disease in RA patients. The levels of TNF-α and IL-1ß in the PDI and the GCF in the concurrent RA and PD group were significantly higher than those in the PD group (P<0.05). Partial correlation analysis showed that TNF-α in the GCF positively correlated with the BOP of patients with RA and PD. Multiple linear regression analysis showed that the level of TNF-α in the GCF and serum CRP were independent influencing factors of the level of IL-1ß in the GCF (the r values were 1.074 and 3.851, respectively; P<0.01). CONCLUSIONS: The presence of RA can increase risk of PD occurrence and is positively correlated with the levels of IL-1ß and TNF-α in the GCF.

Reaction-based colorimetric and ratiometric fluorescence sensor for detection of cyanide in aqueous media.

A stilbene-based compound (1) has been prepared and was highly selective for the detection of cyanide anion in aqueous media even in the presence of other anions, such as F(-), Cl(-), Br(-), I(-), ClO(4)(-), H(2)PO(4)(-), HSO(4)(-), NO(3)(-), and CH(3)CO(2)(-). A noticeable change in the color of the solution, along with a prominent fluorescence enhancement, was observed upon the addition of cyanide. The color change was observed upon the nucleophilic addition of the cyanide anion to the electron-deficient cyanoacrylate group of 1. The spectral changes induced by the reaction were analyzed by comparison with two model compounds, such as compound 2 with dimethyl substituents and compound 3 without a cyanoacrylate group. An intramolecular charge-transfer (ICT) mechanism played a key role in the sensing properties, and the mechanism was supported by DFT/TDDFT calculations.

{N'-[1-(2-Pyrid-yl)ethyl-idene-κN]benzo-hydrazidato-κN',O}{N'-[1-(2-pyrid-yl)ethyl-idene-κN]benzohydrazide-κN',O}copper(II) trichloro-acetate.

In the title complex, [Cu(C(14)H(13)N(3)O)(C(14)H(12)N(3)O)](CCl(3)COO), the central Cu(II) ion exhibits a distorted octa-hedral geometry with the two ligands coordinating in an meridional format. The N(4)O(2) ligand environment is defined by two benzoyl O atoms, two pyridyl N atoms and imino N atoms. As evidenced by the bond lengths, the two benzohydrazone ligands exist in distinctively different forms, one of them as a regular neutral ligand and the other as an anionic enolate arising from deprotonation. The much longer Cu-O bond and longer Cu-N bond lengths in the neutral benzohydrazone ligand imply weak ligation in comparison with the anionic enolate form. The acute angles of the five-membered rings cause a significant deviation from a regular octa-hedral geometry.