Irinotecan injures tight junction and causes bacterial translocation in rat.
J Surg Res
; 173(2): 341-7, 2012 Apr.
Article
em En
| MEDLINE
| ID: mdl-21176921
ABSTRACT
BACKGROUND:
Tight junctions are an essential component of intestinal epithelial barriers. Claudin-1, occludin, and ZO-1 are the components of tight junction. The purpose of this study was to investigate whether irinotecan induces bacterial translocation in rats, and thus elucidate the relationship between tight junction and bacterial translocation.METHODS:
Ten rats were divided into two groups Five were treated with irinotecan and five were not treated with irinotecan, the control group. Irinotecan treated rats were administrated irinotecan 250 mg/kg intraperitoneally on days designated 0 and 1, were then killed at 48 h after treatment, and tissues were collected for analysis. Controls were treated with a saline solution.RESULTS:
In eighty percent of irinotecan treated rats, bacteria were detected in the mesenteric lymph node or spleen. Large intestinal resistance of the rats was decreased. On the contrary, small intestinal resistance increased. Claudin-1 protein expression of both the small and large intestine decreased (P < 0.05), occludin protein expression of the small intestine decreased (P < 0.05), and occludin protein expression of the large intestine had decreasing tendency (P = 0.07) in irinotecan treated rats. In irinotecan treated rats, claudin-1 mRNA of the small intestine decreased (P < 0.05), claudin-1 mRNA of large intestine had a tendency to decrease (P = 0.05), occludin mRNA of both small and large intestine decreased (P < 0.05).CONCLUSIONS:
Irinotecan injures claudin-1 and occludin. It causes disorders in the intestinal epithelial barrier and induces bacterial translocation.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Camptotecina
/
Junções Íntimas
/
Translocação Bacteriana
/
Antineoplásicos Fitogênicos
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Revista:
J Surg Res
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
Japão