Abstract
occluding superior mesenteric artery (SMA) for 45 min. Inflammatory response in the smallintestine(jejunum)wasassessed4hfollowingreperfusionbymeasuringtissuelevelsofTNF-alpha protein (ELISA), histology (Hematoxylin-Eosin stain), iNOS and HO-1 localization(immunohistochemistry), adhesion molecules E-selectin and ICAM-1 (Western blot), NF-kappaB activation (EMSA), and polymorphonuclear neutrophil (PMN) tissue accumulation(MPO assay). iNOS and HO-1 were localized in the epithelium and infiltrated PMN. Theobtained results indicated that tissue levels of TNF-alpha, E-selectin and ICAM-1 proteinexpression, activation of NF-kappaB, and subsequent accumulation of PMN were elevatedin I/R-challenged WT jejunum. The above changes were significantly attenuated in I/R-challenged Bach1 deficient jejunum. Taken together these findings indicate that disruptionof the Bach1 gene resulted in attenuation of I/R-challenged intestinal injury, indicating thatinhibitionofBach1maybeanoveltherapeuticstrategyforthetreatmentagainstI/R-mediatedintestinal injury.
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