Our data collectively indicate that I3M inhibited the production of several inflammatory mediators and might be used for the treatment of various inflammatory diseases.

The effects of sulfate and protein contents as well as molecular weights of the sulfated glycoproteins (NF2) from Codium fragile on the immunomodulation were systematically investigated. The obtained NF2 derivatives displayed various amounts of proteins (2.3-8.7 %) and sulfates (4.3-8.1 %) as well as different molecular weights (47.3-128.0 × 10(3) g/mol). NF2 was not able to stimulate RAW264.7 cells to release NO without its protein moiety, which was essential to activate NF-κB pathway through the degradation and phosphorylation of IκB-α and the subsequent translocation of p65/p50 complex in the cell nucleus. In addition, the proteins in NF2 were required to trigger MAPK pathway for the phosphorylation of ERK1/2, p38, and JNK1/2 as well as the nuclear translocation of c-JUN and c-FOS. However, the protein moiety itself could not activate RAW264.7 cells, thus the complex formation of the polysaccharide and protein moieties in NF2 was pivotal to stimulate macrophage cells.

BackgroundXH-14 isolated from Salvia miltiorrhiza is a bioactive component and adenosine antagonist. In the present study, we evaluated anti-inflammatory properties of XH-14 in murine macrophages.MethodsRAW 264.7 murine macrophage cell line was cultured with various concentrations of XH-14 in the absence or presence of lipopolysaccharide (LPS). LPS-induced release and mRNA expression of inflammatory mediators were examined by ELISA and real-time PCR. The modification of signal pathways involved in inflammatory reactions was determined by Western blotting analysis.ResultsXH-14 suppressed the generation of nitric oxide (NO) and prostaglandin E2, and the expression of inducible NO synthase and cyclooxygenase-2 induced by LPS. Similarly, XH-14 inhibited the release of pro-inflammatory cytokines induced by LPS in RAW 264.7 cells. The underlying mechanism of XH-14 on anti-inflammatory action was correlated with down-regulation of mitogen-activated protein kinase and activator protein-1 activation.ConclusionsXH-14 inhibits the production of several inflammatory mediators and so might be useful for the treatment of various inflammatory diseases.

BackgroundIn dental intravenous sedation, continuous intravenous infusion of a low-dose drug requires an infusion pump such as a syringe pump. To develop a new syringe pump for clinical use, the functions of the pump must meet certain international standards. Various safety and efficacy tests must be performed on the syringe pump, as stipulated by these standards, and an approval must be received from the approving agency based on such test results.MethodsThe authors of the present study developed a novel syringe pump and performed efficacy evaluation by testing its infusion speed at 1 and 25 ml/h, and infusion performance testing at 2 and 24 h. Moreover, performance evaluation was conducted by comparing the novel pump to an existing pump with the infusion speed varied from 1 to 5 ml/h.ResultsIn the efficacy testing on the newly developed syringe pump, infusion with the infusion speed initially set to 1 ml/h resulted in infusion speeds of 1.00 and 0.99 ml/h in the 2- and 24-h assessment, respectively. Changing the infusion speed setting to 25 ml/h resulted in an infusion speed of 25.09 and 23.92 ml/h in the 2- and 24-h assessment, respectively. These results show no significant differences when compared with other commercially available pumps.Conclusions The efficacy testing of the newly developed syringe pump showed the accuracy to be within tolerance. Based on these findings, we believe that the newly developed syringe pump is suitable for clinical use.

Licochalcone, a major phenolic constituent of the licorice species Glycyrrhiza inflata, a constituent of licorice, exhibits various biological properties, including chemopreventive-, antibacterial-, and antispasmodic activities. Recently, Licochalcone E (LicE) was isolated from the roots of Glycyrrhiza inflate, however its biological functions have not been fully examined. In the present study, we investigated the ability of LicE to regulate inflammation reactions in macrophages. Our in vitro experiments using murine macrophages, RAW264.7 cells, showed that LicE suppressed not only nitric oxide (NO) and prostaglandin E2 generation, but also the expression of inducible NO synthase and cyclooxygenase-2 induced by lipopolysaccharide (LPS). Similarly, LicE inhibited the release of proinflammatory cytokines induced by LPS in RAW264.7 cells, including tumor necrosis factor-α and interleukin-6. The underlying mechanism of LicE on anti-inflammatory action correlated with down-regulation of the nuclear factor-κB. Our data collectively indicate that LicE inhibited the production of several inflammatory mediators and might be used in the treatment of various inflammatory diseases.