作者: Ryuji Hayashi , Hiroo Wada , Kazuhiro Ito , Ian M. Adcock
DOI: 10.1016/J.EJPHAR.2004.07.011
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摘要: Abstract Glucocorticoids bind to and activate a cytoplasmic glucocorticoid receptor. The activated receptor translocates into the nucleus binds specific response elements in promoter regions of anti-inflammatory genes such as lipocortin-1 secretory leukocyte protease inhibitor (SLPI). However, major effects glucocorticoids appear be due largely interaction between transcription factors, notably nuclear factor-κB (NF-κB) activator protein-1 (AP-1), that mediate expression inflammatory genes. NF-κB switches on via process involving recruitment transcriptional co-activator proteins changes chromatin modifications histone acetylation. This must occur correct temporal manner allow for effective gene occur. interactions result differing remodelling. Drugs enhance translocation (long acting β-agonists) GR-associated deacetylases activity (theophylline) have been shown add-on therapies. In addition, dissociated target preferentially also successful treatment allergic disease.