There is now a wealth of experimental evidence indicating that the deficit in endogenous
estrogen facilitates the onset of
inflammation that can be antagonized by
estrogen replacement therapy. This work investigated the role of
estrogen in the control of intestinal
inflammation in a panel of
colitis models, focusing on the morphological changes, the activity of mast cells, the expression of
cytokines (IL-1beta, IL-6, and TNF-alpha),
fibronectin and
reactive oxygen species. Two hundred adult male rats were divided into 4 groups:
colitis was induced in Group I and Group II but only the latter was treated with
estrogen; Group III received
estrogen only, and Group IV saline.
Colitis was induced in 4 models using:
iodoacetamide;
iodoacetamide + enteropathogenic E. coli; 2, 4, 6-Trinitrobenzene
sulfonic acid; and
dextran sulfate sodium salt. Macroscopic and microscopic evaluations of abdominal structures as well as molecular analysis were made on days 7, 14, 28 and 56. There was a significant improvement in the health condition of the
estrogen-treated rats: the
inflammation scores were reduced by at least 10-15%, the number of mast cells in the colon decreased by 30%,
fibronectin expression was only 50% and
reactive oxygen species decreased by 30%. In addition, there was a significant decrease in
TNF-alpha,
IL-6 and IL-1beta expression by about 25%. In conclusion, there was an improvement in the inflammatory status in all
estrogen-treated groups through the duration of the experiment at all-time points. In addition, there was less tissue
necrosis as depicted by less
fibronectin and a marked
antioxidant effect.