Polynitroxylated starch/TPL attenuates cachexia and increased epithelial permeability associated with TNBS colitis.

摘要: Free radicals play an important role in the initiation and progression of inflammatory bowel disease (IBD). Therefore, reduction or elimination adverse oxidant effects can provide novel therapy for IBD. Here, antioxidant capacity protective a new class chemically modified hetastarch (polynitroxyl starch, PNS) plus 4-hydroxyl-2,2,6,6-tetramethylpiperidine-N-oxyl (Tempol TPL) (PNS/TPL) were assessed model colitis. The superoxide scavenging PNS/TPL—that is, inhibition cytochrome c presence xanthine/xanthine oxidase (X/XO)—was evaluated vitro. PNS/TPL on X/XO–induced neutrophil endothelial adhesion vitro investigated. Also, this study tested protection produced by mouse trinitrobenzene sulfonic acid (TNBS)–induced was given intravenously immediately before (<30 min) intraperitoneally at 24 72 hr after TNBS induction. body weight survival rate mice checked daily. Colonic mucosal damage 7th day measuring intestinal permeability to Evans blue (EB) vivo. ability PNS reoxidize bioreduced TPL documented whole-body electron paramagnetic resonance (EPR) detection. We found that exhibits dismutase (SOD)–like activity, with approximately 2% SOD activity occurring molar basis. endothelial–neutrophil adherence induced X/XO significantly inhibited but not alone. protected against cachexia mortality, both usually TNBS. Epithelial increased ameliorated administration PNS/TPL. In conclusion, may be beneficial treatment prevention IBD through its effects, which inhibit oxidant-mediated leukocyte injury cells.