to Much hour ago. Thus, all results were compared to celecoxib selenocoxibs parent. In addition to their inhibitory effect on COX-2 activity T of LPS in macrophages, such as by a decrease of TXB2 and PGE2-induced shown selenocoxibs also inhibited the expression of COX-2 in prime Ren and immortalized macrophages stimulated with LPS. In general, two clearly distinguishable selenocoxib induces a potent inhibitor of COX-2 by LPS, TNF, and the expression of iNOS 0.1 million to LPS treated DMSO embroidered on celecoxib or 3 groups compared selenocoxib. Although less POWERFUL compatibility available as selenocoxib 2 selenocoxib 3 has also been found in some iNOS Ma S to 1 M inhibit, but not at 0.1 M. This effect was not observed egfr in the case of COX-2 expression. Although the reason for the differential effect is not clear, we believe that the 3 selenocoxib expected the upstream Rts signal transduction pathways have is to modulate the expression of iNOS in high concentrations. The fact that NF ? B regulates the expression of COX-2, TNF and prompted iNOS in macrophages of the LPS model inflammation us examine in the modulation of NF ? B Activation of these derivatives celecoxib. We found that 2 inhibits NF selenocoxib ? B, w During selenocoxib 3, no inhibition by LPS in perceptible ? NF B binding was induced. Thus, it is very likely that the mechanism of down-regulation of COX-2 and iNOS expression probably mediated by both selenocoxibs by different mechanisms. Recent studies have shown that additionally Tzlich I ? to inhibit kinase B, celecoxib is also the activity of t The upstream Rtigen kinases act as affected.
Although these concentrations THE RESIDENCE Nglichen are also with high doses of celecoxib, it is particularly interesting that Akt inhibitors show the struggle against the metastatic potential of tumor cells, in part, dependent by the down-regulation of NF B expression ?-Dependent gene. Also obtained ht Studies by Desai et al analog in the power of this inhibitor of iNOS PBIT, additionally Tzlich to the PI3 kinase Akt inhibition and apoptosis Cilomilast in a variety of cancer cell lines. Thus, the decreased phosphorylation substrate IKK, I B GST ? highlighted in macrophages treated with selenocoxib 2 k Nnte probably due to modulation of the upstream Rtigen signal components of the NF-B signaling axis ? which reduces to the expression downstream Rts target genes. To explained to Ren why only selenocoxib 2 was effective, we hypothesized that the release of this molecule was down-regulation of NF B. Cause probably ? Previous studies in our laboratory have to reverse a causal relationship between the status of Se in macrophages and NF-B dependent-dependent expression of the proinflammatory gene ? abh demonstrates-dependent synthesis of selenoproteins. GPX1 reduces reactive oxygen species in the cells, and thus the induced upregulation of oxidative stress by pro inflammatory genes. Unlike p XSC where hydrogen selenide is formed during metabolism in rodents, but not in st Stoichiometric amounts of selenocoxib published 2 by cytochrome P450 enzyme systems, such as CYP2C9, celecoxib is known to metabolize seen. Based on the analysis of semi-quantitative Western blot, beautiful we tzten about 2 seconds available for the installation was in GPX1, which usually ? not sufficient for down-regulation of NF B pathway. Alternatively, it is also