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Start Over Author "Han, Xin-Bing" Journal pediatric research
3 results on '"Han, Xin-Bing"'

2. Inhibition of Nuclear Factor-?B Ameliorates Bowel Injury and Prolongs Survival in a Neonatal Rat Model of Necrotizing Enterocolitis

Author

De Plaen, Isabelle G, Liu, Shirley X L, Tian, Runlan, Neequaye, Isaac, May, Michael J, Han, Xin-Bing, Hsueh, Wei, Jilling, Tamas, Lu, Jing, and Caplan, Michael S

Abstract

Necrotizing enterocolitis (NEC) is a major cause of morbidity and death in premature infants. NEC is associated with increased levels of pro-inflammatory cytokines in plasma and tissues that are regulated by the transcription factor nuclear factor-?B (NF-?B). It remains unknown, however, whether NF-?B mediates injury in neonatal NEC. We therefore examined the activation status of NF-?B perinatally in the small intestine and in a neonatal rat model of NEC. We found that intestinal NF-?B is strongly activated at birth and, in dam-fed newborn rats, is down-regulated within a day. In contrast, NF-?B remains strongly activated at both d 1 and d 2 in stressed animals, and this is accompanied by a significant decrease in the levels of the endogenous NF-?B inhibitor protein I?Ba and I?Bß at d 2. To determine the importance of elevated NF-?B activity in intestinal injury in NEC, we administered the NEMO-binding domain (NBD) peptide that selectively inhibits the critical upstream I?B kinase (IKK). NBD but not a control peptide decreased mortality and bowel injury in this model, supporting the hypothesis that bowel injury in NEC results from elevated NF-?B activity. Our findings therefore lead us to conclude that selective NF-?B inhibition represents a promising therapeutic strategy for NEC.

Published
2007
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3. Inhibition of nuclear factor-kappaB ameliorates bowel injury and prolongs survival in a neonatal rat model of necrotizing enterocolitis.

Author

De Plaen IG, Liu SX, Tian R, Neequaye I, May MJ, Han XB, Hsueh W, Jilling T, Lu J, and Caplan MS

Subjects
Animals, Animals, Newborn, Disease Models, Animal, Enterocolitis, Necrotizing pathology, Intestinal Mucosa metabolism, Intestines drug effects, Intestines pathology, Nitric Oxide Synthase Type II analysis, Nitric Oxide Synthase Type II metabolism, Rats, Rats, Sprague-Dawley, Enterocolitis, Necrotizing drug therapy, NF-kappa B antagonists & inhibitors, Peptides therapeutic use
Abstract

Necrotizing enterocolitis (NEC) is a major cause of morbidity and death in premature infants. NEC is associated with increased levels of pro-inflammatory cytokines in plasma and tissues that are regulated by the transcription factor nuclear factor-kappaB (NF-kappaB). It remains unknown, however, whether NF-kappaB mediates injury in neonatal NEC. We therefore examined the activation status of NF-kappaB perinatally in the small intestine and in a neonatal rat model of NEC. We found that intestinal NF-kappaB is strongly activated at birth and, in dam-fed newborn rats, is down-regulated within a day. In contrast, NF-kappaB remains strongly activated at both d 1 and d 2 in stressed animals, and this is accompanied by a significant decrease in the levels of the endogenous NF-kappaB inhibitor protein IkappaBalpha and IkappaBbeta at d 2. To determine the importance of elevated NF-kappaB activity in intestinal injury in NEC, we administered the NEMO-binding domain (NBD) peptide that selectively inhibits the critical upstream IkappaB kinase (IKK). NBD but not a control peptide decreased mortality and bowel injury in this model, supporting the hypothesis that bowel injury in NEC results from elevated NF-kappaB activity. Our findings therefore lead us to conclude that selective NF-kappaB inhibition represents a promising therapeutic strategy for NEC.

Published
2007
Full Text
View/download PDF

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