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COPD, inflammation and anti-inflammatory Research


D in patients with sputum concentrations of interleukin-l0 lower than normal, which may increase the inflammatory response in the mechanism of pneumonia. IL-10 has recently been used to treat other chronic inflammatory diseases in clinical trials (such as inflammatory bowel disease, rheumatoid arthritis and psoriasis),[link widoczny dla zalogowanych], including steroid-resistant patients, but it has side effects caused by blood diseases. IL-10 in the treatment of COPD. Especially in the future development of selective receptor agonist and its unique signaling pathway around after,[link widoczny dla zalogowanych], there will be some potential therapeutic value. (10) INOS inhibitor of oxidative stress and increased release from INOS reaction of nitrogen oxides, can lead to the formation of peroxynitrite ions, which ions can cause protein nitration and functional changes. 3-nitro-tyrosine reflect a ring nitrogen oxide formation. It ('() PI) in sputum macrophages significantly increased the amount. Selective iNOS inhibitors are under development. One is the precursor of lysine l one by one. Stable and lasting reduction in exhaled air concentrations of nitrogen oxides. (11) FB NFB regulation of interleukin inhibitor 8, TNFa, and inflammatory cytokines, and some MMP expression. FB in C () PD patients with macrophages and epithelial cells are activated. Especially when the condition deteriorated. FB activity may inhibit the gene conversion methods include IB, IKK inhibitors, FI3 induced kinase. Common to adjust the NFB ligase activity and can inhibit IB IB degradation of the drug. The most promising method is to use small molecule inhibitors to inhibit IKK2, some of them are under development. A small molecule IKK2 inhibitor, can inhibit the release of alveolar macrophage inflammatory cytokines and chemical factors, which may be effective because of COPD alveolar macrophages on the anti-inflammatory effects of corticosteroids are resistant. However. Long-term suppression of FB can lead to immune suppression and host defense weakened. Gene in mice because of the lack FB will die of sepsis. Therefore, another kinase rather than through the IKK pathway may be activated FI3 the more important in the inflammatory lesions. (12) P38MAPK inhibitor of MAPK in chronic inflammation plays an important role. Some of the complex cascade of enzymes has now been elucidated. Them. P38MAPK pathway, is activated by cellular stress response and regulates the expression of inflammatory cytokines, including interleukin-8, TNFa and MMP. P38MAPK small molecule inhibitors such as SB203580, SB239063, and RWJ67657,[link widoczny dla zalogowanych], a wide range of anti-inflammatory effect. SB239063 can reduce the inhalation of endotoxin after the infiltration of neutrophils. And to reduce the rat bronchial lavage fluid IL-6 and the concentration of MMP9. All this shows that it is in the treatment of COPD as an anti-inflammatory drugs are potentially valuable applications. With such a broad anti-inflammatory drugs is likely to produce a toxic side effect, but by inhalation is a feasible way. (13) PI3 ~ inhibitor of PI3 regulate cell activity can cause some of the activities of the generation of lipid second messengers. One of the very special subtype PI37, it neutrophil recruitment and activation of cells related to the process. Excluding the genes of this subtype can inhibit neutrophil migration and activation. At the same time weaken the T cell and macrophage function. So. Selective inhibitors may PI37 C () PD to play the appropriate anti-inflammatory effect. PI37 and PI36 of small molecule inhibitors are being studied. (14) PPAR agonists PPARs is a steroid receptor superfamily of ligand activated nuclear hormone receptor family, which has been found in three widely expressed isoforms a, 7,6. The evidence suggests that activation of PPARa and PPAR7 have anti-inflammatory and immune regulatory role. Such as troglitazone that PPARa agonists,[link widoczny dla zalogowanych], can inhibit the inflammatory cytokines released from mononuclear cells. And induced T cell apoptosis. This all suggest that they can play in the anti-inflammatory COPD. 3 We need the future direction of the development of new drugs to treat COPD. However, to prove that the new method of treatment in delaying effect on the lung function damage will be very difficult. Because it requires at least 3 years of extensive research. The current development of drugs such as PDE4 inhibitors, p38MAPK inhibitors and CXCR2 inhibitor, there is hope in the next 5 to 10 years as anti-inflammatory drugs for clinical use. Effective anti-inflammatory treatment can not only alleviate the progression of disease,[link widoczny dla zalogowanych], but also improve the symptoms and health status. The long term, these drugs can delay the decline in lung function and the elimination of the common diseases of potential risk of death. r Received :2005-02-08]