Inflammatory alterations in excluded colon in rats: A comparison with chemically induced colitis

被引:13
作者
Longatti, Thamara Sigrist [1 ]
Acedo, Simone Coghetto [1 ]
De Oliveira, Caroline Candida [1 ]
Da Conceicao Miranda, Daniel Duarte [1 ]
Priolli, Denise Goncalves [1 ]
Ribeiro, Marcelo Lima [1 ]
Gambero, Alessandra [1 ]
Real Martinez, Carlos Augusto [1 ]
机构
[1] Univ Sao Francisco, Sch Med, Clin Pharmacol & Gastroenterol Unit, BR-12916900 Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
CHAIN FATTY-ACIDS; FACTOR-KAPPA-B; DIVERSION COLITIS; DNA-DAMAGE; INHIBITION; PROCTITIS;
D O I
10.3109/00365520903471572
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Diversion colitis occurs commonly in the large bowel remnant after diversion of the fecal stream. Several experimental models of colitis have been described, but none examine the inflammatory alterations that can occur in experimentally defunctioned colons. This characterization could be useful in understanding pathophysiological aspects of diversion colitis, and in developing future therapeutic strategies. Thus, we evaluated the temporal inflammatory alterations in the defunctioned colon of rats by analyzing the histological results, infiltrating neutrophils, pro-inflammatory markers such as cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS), and DNA damage in isolated colonocytes. We compared the obtained data with those from hapten-induced colitis. The experimental diversion of the colon fecal stream induces diversion colitis characterized by an early inflammatory process with increased neutrophil infiltrate, and COX-2 and iNOS expression that resembles, in some aspects, the inflammatory characteristics of chemically induced colitis. After acute inflammation resolution, there was an increase in COX-2 and iNOS expression and the presence of lymphoid follicular hyperplasia and ulcerations, suggesting that diversion colitis can be experimentally established and useful for studying different pathophysiological aspects of this condition.
引用
收藏
页码:315 / 324
页数:10
相关论文
共 35 条
[1]   Inducible nitric oxide synthase from bone marrow-derived cells plays a critical role in regulating colonic inflammation [J].
Beck, Paul L. ;
Li, Yan ;
Wong, J. ;
Chen, Chang-Wen ;
Keenan, Catherine M. ;
Sharkey, Keith A. ;
McCafferty, Donna-Marie .
GASTROENTEROLOGY, 2007, 132 (05) :1778-1790
[2]   MEASUREMENT OF CUTANEOUS INFLAMMATION - ESTIMATION OF NEUTROPHIL CONTENT WITH AN ENZYME MARKER [J].
BRADLEY, PP ;
PRIEBAT, DA ;
CHRISTENSEN, RD ;
ROTHSTEIN, G .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1982, 78 (03) :206-209
[3]   Curcumin, a Curcuma longa constituent, acts on MAPK p38 pathway modulating COX-2 and NOS expression in chronic experimental colitis [J].
Camacho-Barquero, Laura ;
Villegas, Isabel ;
Sanchez-Calvo, Juan Manuel ;
Talero, Elena ;
Sanchez-Fidalgo, Susana ;
Motilva, Virginia ;
de la Lastra, Catalina Alarcon .
INTERNATIONAL IMMUNOPHARMACOLOGY, 2007, 7 (03) :333-342
[4]   Intraluminal irrigation with fibers improves mucosal inflammation and atrophy in diversion colitis [J].
de Oliveira-Neto, JP ;
de Aguilar-Nascimento, JE .
NUTRITION, 2004, 20 (02) :197-199
[5]   Attenuation of Colitis Injury in Rats using Garcinia cambogia Extract [J].
dos Reis, Samara Bonesso ;
de Oliveira, Caroline Candida ;
Acedo, Simone Coghetto ;
da Conceicao Miranda, Daniel Duarte ;
Ribeiro, Marcelo Lima ;
Pedrazzoli, Jose, Jr. ;
Gambero, Alessandra .
PHYTOTHERAPY RESEARCH, 2009, 23 (03) :324-329
[6]  
Edwards CM, 1999, HISTOPATHOLOGY, V34, P1
[7]  
GLOTZER DJ, 1981, GASTROENTEROLOGY, V80, P438
[8]   Histologic inflammation is a risk factor for progression to colorectal neoplasia in ulcerative colitis: A cohort study [J].
Gupta, Roopali Bansal ;
Harpaz, Noam ;
Itzkowitz, Steven ;
Hossain, Sabera ;
Matula, Sierra ;
Kornbluth, Asher ;
Bodian, Carol ;
Ullman, Thomas .
GASTROENTEROLOGY, 2007, 133 (04) :1099-1105
[9]   TREATMENT OF DIVERSION COLITIS WITH SHORT-CHAIN FATTY-ACID IRRIGATION [J].
HARIG, JM ;
SOERGEL, KH ;
KOMOROWSKI, RA ;
WOOD, CM .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 320 (01) :23-28
[10]   Inhibition of RICK/nuclear factor-κB and p38 signaling attenuates the inflammatory response in a murine model of Crohn Disease [J].
Hollenbach, E ;
Vieth, M ;
Roessner, A ;
Neumann, M ;
Malfertheiner, P ;
Naumann, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (15) :14981-14988