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김원호 ( Won Ho Kim ),박인혜 ( In Hye Park ),조재희 ( Jae Hee Cho ),김태일 ( Tae Il Kim ) 대한장연구학회 2003 Intestinal Research Vol.1 No.1
Most of patients with ulcerative colitis have intermittent chronic disease demonstrating recurrent flare-ups of bloody diarrhea and symptom-free periods. Sulfasalazine and mesalazine are the first-line medical therapy in patients with mild to moderate activity, as both of them are effective in inducing and maintenance of remission. However, significant proportion of patients needs stronger drugs such as corticosteroids. As corticosteroids are ineffective for the prevention of relapse and associated with frequents side-effects, immunosuppressors, 6-mercaptopurine (6-MP) and its prodrug azathioprine, have been used in selected patients. After absorption azatioprine is rapidly converted to 6-MP non-enzymatically and 6-MP is either inactivated by thiopurine methyltransferase (TPMT) to 6-methylmercaptopurine or by xanthine oxidase to 6-thiouric acid, or it is activated via a multistep enzymatic pathway to the putative active metabolites, 6-thioguanine nucleotides (6-TGN). Clinical responsiveness and side effects are associated with TPMT genotype and phenotype, because the enzymatic activity of TPMT is genetically determined. Until now, significant proportion of patients with proper indication are not receiving immunosuppressors because of safety concern and delayed onset of action. Recently, however, gastroenterologists`` acceptance for immunomodulators is increasing based on favorable results regarding efficacy and safety. The recent application of the study of variability in drug response due to genetic factors, termed pharmacogenetics, has provided a chance for tailored dosing in the individual patients. (Intestinal Research 2003;1:5-18)
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판철호,김은선,엄병헌,이재권 대한약학회 2011 Archives of Pharmacal Research Vol.34 No.4
Flavonoids have biological activities including anti-allergic, anti-inflammatory, antimicrobial and anticancer activities shown from in vitro studies. Of these biological activities, the antiinflammatory capacity of flavonoids has long been emphasized in Chinese medicine. In this study, I investigated that what flavonoid can be applied to the suppression of lipopolysaccharide (LPS)-induced inflammatory responses in macrophages among the four similar structure flavonoids. Eriodictyol was found to reduce nitric oxide (NO) production from LPS-stimulated Raw 264.7 cells in non-cytotoxic concentrations. Moreover, eriodictyol strongly suppressed the phagocytic activity of activated macrophages. Pre-treatment of Raw 264.7 cells with eriodictyol reduced the expression of mRNA and the secretion of pro-inflammatory cytokines. These inhibitory effects were found to be caused by blockage of nuclear factor kappa-light-chainenhancer of activated B cells (NF-κB) activation and phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun Nterminal kinase (JNK).
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Anti-inflammatory Effect of Trichostatin-A on Murine Bone Marrow-derived Macrophages
한상배,이재권 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.4
Histone deacetylase (HDAC) inhibitors were recently shown to suppress inflammatory responses in models of autoimmune and inflammatory diseases. In this study, the anti-inflammatory effects of five different HDAC inhibitors on lipopolysaccharide-(LPS)-stimulated macrophages were compared and the mechanisms of these effects were demonstrated. Trichostatin-A (TSA) and scriptaid, two of the five HDAC inhibitors, showed the most potent inhibitory effects on the nitric-oxide (NO) production of RAW264.7 cells and bone-marrowderived macrophages (BMDMs). TSA significantly decreased the mRNA and protein levels of the proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β, whereas the pretreatment with TSA increased the level of the immunosuppressive cytokine IL-10. TSA also reduced the cell surface markers of the maturity of the macrophages. Furthermore, a longer duration (up to 8 h) of hyperacetylation was observed in the cells that had been exposed to TSA, whereas the hyperacetylation induced by the other HDAC inhibitors was absent after 8 h. These results demonstrated that TSA is the most potent HDAC inhibitor of histone deacetylation and has the greatest ability to induce anti-inflammatory activity in cloned and naïve macrophages. These results are expected to serve as a guide for future studies on the ability of HDAC inhibitors to inhibit acute and chronic inflammatory diseases.
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Noh, Kyung Tae,Jung, In Duk,Cha, Gil Sun,Han, Myung-Kwan,Park, Yeong-Min American Society for Biochemistry and Molecular Bi 2017 The Journal of biological chemistry Vol.292 No.8
<P>Indoleamine 2,3-dioxygenase (IDO) mediates immune tolerance, and suppressor of cytokine signaling 3 (SOCS3) negatively regulates the JAK/STAT signal transduction pathway. We determined previously that platelet-activating factor (PAF) protects mice against LPS-induced endotoxic shock, but its detailed mechanism of action was unknown. We performed survival experiments in IDO+/+ and IDO-/- mice using an LPS-induced endotoxemia model and rated organ injury (neutrophil infiltration and liver function). Using ELISA and Western blotting, we also investigated the mechanism of PAF-mediated endotoxin tolerance during endotoxemia. PAF-mediated endotoxin tolerance was dependent on IDO in vivo and in vitro and was not observed in IDO-/- mice. JAK/STAT signaling, crucial for SOCS3 expression, was also impaired in the absence of IDO. In an IDO- and STAT-dependent manner, PAF mediated a decrease in IL-12 and a dramatic increase in IL-10 and reduced mouse mortality. In addition, PAF attenuated LPS-mediated neutrophil infiltration into the lungs and interactions between neutrophil-like (THP-1) and endothelial cells (human umbilical vein endothelial cells). These results indicate that PAF-mediated endotoxin tolerance is initiated via IDO- and JAK/STAT-dependent expression of SOCS3. Our study has revealed a novel tolerogenic mechanism of IDO action and an important association between IDO and SOCS3 with respect to endotoxin tolerance.</P>
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