Chrysin NO production in the muscularis as a mechanism

for ver Nderten motility t And dilation, the hallmark of toxic megacolon.22 25 Interestingly, is embroiled may cortico Do not seem to reduce the expression of NO synthase mucosal ulcerative colitis patients 0.26 These results are in accordance with the observation that some pathogenic bacteria induced NO production in intestinal Chrysin epithelial cells by a mechanism dependent,-Dependent is NF ?B but corticosteroids insensitive and Schlu clusion because the reduction of curcumin dependent-dependent epithelial cell NO production resulting from 28 activation.27 is NF ? ?B ??berm strength NO production can inflammation.
29 mucosal inflammation caused by the formation of intermediates, such as peroxynitrite Ridaforolimus and cause intrarectal instillation rats peroxynitrite trinitro benzenesulfonic acid-induced colitis in rats is increased by strong hte NO production, and this interference model was marked with NO production by the oral administration of L NAME impressive protective layer 31 effects.30 However, it is well known that NO also Ma took protection of TNBS-induced colitis and treatment with L NAME before the induction of colitis, erh hte mucosal 0.32 The Similar observations have been reported in human HLA B27 ? Been microglobulin transgenic rats and conflicting data ffentlicht ver, The effectiveness of the NO inhibitor aminoguanidine in TNBS-induced NO release colitis.
33 35 A preparation of mesalazine was superior in a rat model of colitis and mesalazine inhibits adhesion Sion of neutrophils and the production of IL-1 and interferon ? ?? ? 36 In colitis in rhesus monkeys spontaneously occurring, the management of various inhibitors of inducible NO synthase MODIFIED Alter the clinical outcome has NO severity.37 In many physiological functions of the human intestine, and NO production by intestinal epithelial cells through inducible NO synthase is often observed in the non-diseased bowel.38 At high concentrations, NO can Sch the. to the intestinal mucosa, with the formation of intermediate products such as peroxynitrite It is extremely difficult, a therapeutic strategy that targets only one above the design Owned production of NO, and the beautiful dlichen effects of NO blockade and protection has been observed in animal models. For this reason it is unlikely that the currently available blockers are effective in inflammatory bowel disease, but no clinical data were reported.
PPAR ? ?? ? ?P eroxisome proliferator-activated receptor ? ?? ? Is a nuclear receptor that was originally identified as an important regulator of adip Sen differentiation and metabolism, and sp Ter as a receptor for immunity t and inflammation.39 stimulating PPAR ? ?? ? ?i n macrophage inhibition of nuclear factor ? ?B that with the induction of apoptosis 0.40 additives assigned tzlich, activation of PPAR ? ?? ? ?? auses inhibition of AP and STAT 1 signaling pathways, and at the same time explained rt PPAR ? ?? ? ?m ediated reduction of IL-2, IL -6, IL-8, TNF ? IL 12 and 42 metalloproteinase release.41 These results may be important for inflammatory bowel disease, because The lining of the heart lon express high PPAR ?43 44 M Nozzles, which are deficient in PPAR ? Retinal or receptor RXR, which is a heterodimer PPAR ? ?? ? ?p artner, exhibit increased