TY - JOUR
T1 - Induction of heme oxygenase-1 improves impaired intestinal transit after burn injury
AU - Gan, Hua Tian
AU - Chen, J. D.Z.
PY - 2007/3/1
Y1 - 2007/3/1
N2 - Background: Burn injury has been shown to impair intestinal transit. The induction of heme oxygenase (HO)-1, the rate-limiting enzyme in heme degradation, has been demonstrated to provide protection against various injuries. The aim of this study was to investigate whether the induction of HO-1 by hemin would improve impaired intestinal transit after burn injury. Methods: Burn/sham rats were divided into 3 groups: saline solution, hemin (HO-1 inducer), and hemin plus tin protoporphyrin IX. Intestinal transit was measured with the use of phenol red and assessed with the geometric center. The gene and/or protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, interleukin (IL)-1β, HO-1, and p38 mitogen-activated protein kinase (p38 MAPK) was measured by real-time polymerase chain reaction and/or by Western blot analysis. Results: Intestinal transit was delayed with burn injury and improved significantly with the induction of HO-1; burn injury significantly activated p38 MAPK and myeloperoxidase and increased gene and/or protein expression of iNOS, COX-2, IL-1β, and HO-1. The administration of hemin led to a significant decrease in the activation of p38 MAPK and myeloperoxidase and the gene and/or protein expression of iNOS, COX-2, and IL-1β. Conclusion: The induction of HO-1 improves burn-induced delayed intestinal transit. The beneficial effect of hemin treatment could be linked, at least in part, to the down-regulation of iNOS, COX-2, and IL-1β expression, which suggests that the induction of HO-1 may provide an effective therapeutic measure for gut dysmotility after burn injury.
AB - Background: Burn injury has been shown to impair intestinal transit. The induction of heme oxygenase (HO)-1, the rate-limiting enzyme in heme degradation, has been demonstrated to provide protection against various injuries. The aim of this study was to investigate whether the induction of HO-1 by hemin would improve impaired intestinal transit after burn injury. Methods: Burn/sham rats were divided into 3 groups: saline solution, hemin (HO-1 inducer), and hemin plus tin protoporphyrin IX. Intestinal transit was measured with the use of phenol red and assessed with the geometric center. The gene and/or protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, interleukin (IL)-1β, HO-1, and p38 mitogen-activated protein kinase (p38 MAPK) was measured by real-time polymerase chain reaction and/or by Western blot analysis. Results: Intestinal transit was delayed with burn injury and improved significantly with the induction of HO-1; burn injury significantly activated p38 MAPK and myeloperoxidase and increased gene and/or protein expression of iNOS, COX-2, IL-1β, and HO-1. The administration of hemin led to a significant decrease in the activation of p38 MAPK and myeloperoxidase and the gene and/or protein expression of iNOS, COX-2, and IL-1β. Conclusion: The induction of HO-1 improves burn-induced delayed intestinal transit. The beneficial effect of hemin treatment could be linked, at least in part, to the down-regulation of iNOS, COX-2, and IL-1β expression, which suggests that the induction of HO-1 may provide an effective therapeutic measure for gut dysmotility after burn injury.
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U2 - 10.1016/j.surg.2006.06.023
DO - 10.1016/j.surg.2006.06.023
M3 - Article
C2 - 17349851
AN - SCOPUS:33847763251
SN - 0039-6060
VL - 141
SP - 385
EP - 393
JO - Surgery
JF - Surgery
IS - 3
ER -