EA is the most hours Ufigsten TGF-beta used formulation of the receiver Ngnisverhütung and, together with its use in HRT, women provide more than 10 million years after the exposure to market reassuring evidence for the efficacy reps Opportunity and security DNG. DNG data for the treatment of endometriosis itself suggest a favorable safety and reps Glichkeitsprofil. The h Ufigsten side effects were nonspecific and Resemble those of other studies of progestins in the COC, including normal bleeding, reinforcing Rkung headaches, mood swings or depression, chest discomfort, abdominal pain, acne and weight. Dropout rates were associated with adverse events have always been low in clinical studies of DNG. 6th Conclusion of its chemical structure is a progestin DNG Ybrid What has pharmacodynamic properties typical of the two main classes of progestins, but also some more specific properties. LPS/HMGB1 induction of all these cytokines in a dose-way Girlfriend. Similar effects were observed after treatment with inhibitors of progesterone, an endogenous ligand for the PR. Because TLR4 expression has been reported to be regulated by ligands of TLR4, we examined the effect of LPS/HMBG1 on TLR4 mRNA content. LPS/HMGB1 to TLR4 mRNA regulated and this regulation was significantly inhibited by up to DNG and progesterone. In EM E6/E7/TERT parental cells, the low PR, no inhibitory effect of progesterone or DNG observed expressed. Since the induction of IL-8 production by LPS/HMGB1 and the inhibitory effect of DNG is an increase TLR4 mRNA expression, we were assuming that TLR4 was necessary to control for the induction of IL 8 LPS/HMGB1 We analyzed the R From the up-regulation of TLR4 in IL-8 production by transient transfection of PR withTLR4siRNAto knockdownTLR4 EM cells. IL-8 production induced LPS/HMGB1 was steamed Mpft by the inactivation of TLR4. SiRNAwas best Preferential specificity of the t using the scrambled siRNA transfectants. These results suggest that DNG LPS/HMGB1 inhibits IL 8 by inhibiting the production of TLR4-induced regulation. Since the stimulation of TLR4 signaling activates transcription factors like NF-kB, we have yet whether LPS / NF-kB signaling HMGB1 modulated determined. The NF-kB inhibitor Bay11 inhibited TLR4 mRNA LPS/HMGB1 until 7082 by the Regulation. In addition, the treatment induces NF-kB LPS/HMGB1 high activity t using a reporter assay, NF-kB, steamed mpft And the DNG-induced NF-kB activity t. Discussion In this study, we showed that TLR4 LPS/HMGB1 regulated gene expression in HEEC up, which was followed by the production of IL 8th In addition wedemonstrated thatLPS/HMGB1 inducedTLR4 the regulation and the subsequent End production of IL-8 was inhibited by DNG on the PR. LPS/HMGB1 inducing the production of other cytokines downstream Rts of TLR4 and IL-6, MCP-1 was also inhibited by the DNG format. To our knowledge this is the first report of a PR agonist can kill expression of TLR4 mRNA to inhibit endometrial cells. TLR4 induction of IL-6 and tumor necrosis factor production have been reported in peritoneal macrophages from patients with endometriosis in vitro. Since the level of inflammatory factors in the endometrial tissue in which TLR4 expression is high and if obtained Ht it will be much TLR4 agonists.