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Am J Physiol Gastrointest Liver Physiol 283: G27-G36, 2002. First published February 20, 2002; doi:10.1152/ajpgi.00460.2001
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Vol. 283, Issue 1, G27-G36, July 2002

Modulatory effects of estrogen in two murine models of experimental colitis

Elena F. Verdú, Yikang Deng, Premysl Bercik, and Stephen M. Collins

Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario L8N 3Z5, Canada

The association between oral contraceptives or pregnancy and inflammatory bowel disease is unclear. We investigated whether 17beta -estradiol modulates intestinal inflammation in two models of colitis. Female mice were treated with 17beta -estradiol alone or with tamoxifen, tamoxifen alone, 17alpha -estradiol, or placebo. Dinitrobenzene sulfonic acid (DNB)- or dextran sodium sulfate (DSS)-induced colitis were assessed macroscopically, histologically, and by myeloperoxidase (MPO) activity. Malondialdehyde and mRNA levels of intercellular adhesion molecule-1 (ICAM-1), interferon-gamma (IFN-gamma ), and interleukin-13 (IL-13) were determined. In DNB colitis, 17beta -estradiol alone, but not 17beta -estradiol plus tamoxifen, or 17alpha -estradiol reduced macroscopic and histological scores, MPO activity and malondialdehyde levels. 17beta -Estradiol also decreased the expression of ICAM-1, IFN-gamma , and IL-13 mRNA levels compared with placebo. In contrast, 17beta -Estradiol increased the macroscopic and histological scores compared with placebo in mice with DSS colitis. These results demonstrate anti-inflammatory and proinflammatory effects of 17beta -estradiol in two different models of experimental colitis. The net modulatory effect most likely reflects a combination of estrogen receptor-mediated effects and antioxidant activity and may explain, in part, conflicting results from clinical trials.

inflammation; antioxidant activity; sex steroids


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