Anti-thyroid drugs decrease mucosal damage in a rat model of experimental colitis

Aliment Pharmacol Ther. 1997 Apr;11(2):341-5. doi: 10.1046/j.1365-2036.1997.127299000.x.


Background: Methimazole, an anti-thyroid drug, was recently found to be useful in the treatment of systemic lupus erythematosus and other autoimmune diseases. Moreover, decreased thyroid hormone production is associated with a variety of immunological manifestations, such as reduced activation of CD4+ cells, increased CD8+ cell activity and reduced soluble IL-2 receptors. In the present study we examined the effects of methimazole and propylthiouracil on a rat model of experimental colitis.

Methods: Colitis was induced by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB). Two weeks prior to induction of colitis, rats were treated by either methimaziole (0.04%) or propylthiouracil (0.01%) in drinking water after a week of free access to water. Rats were sacrificed 48 h or 7 days after induction of colitis. The colon was isolated, rinsed with ice-cold water and weighed. Damage was assessed both macroscopically and microscopically and myeloperoxidase (MPO) activity determined.

Results: All treated rats were hypothyroid as manifested by a significant elevation of thyroid stimulating hormone (TSH), by comparison with the control groups (mean -1.82 +/- 0.40 versus 0.11 +/- 0.02 mmol/L, respectively). The inflammatory response elicited by TNB resulted in severe mucosal damage 48 h after damage induction, which persisted for 7 days. Pre-treatment with either methimazole 0.04% or propylthiouracil 0.01% significantly decreased mucosal damage macroscopically (lesion area, lesion score and segmental weight) microscopically and also significantly decreased MPO level at both time points (P < 0.01).

Conclusions: Methimazole and propylthiouracil significantly reduce mucosal damage and colonic weight in a rat model of colitis. The mode by which they do so remains to be studied.

MeSH terms

  • Animals
  • Antithyroid Agents / pharmacology*
  • Colitis, Ulcerative / chemically induced
  • Colitis, Ulcerative / pathology
  • Colitis, Ulcerative / prevention & control*
  • Intestinal Mucosa / drug effects*
  • Intestinal Mucosa / enzymology
  • Intestinal Mucosa / pathology
  • Male
  • Methimazole / pharmacology
  • Necrosis
  • Peroxidase / metabolism
  • Propylthiouracil / pharmacology
  • Rats
  • Rats, Inbred Strains
  • Trinitrobenzenesulfonic Acid / toxicity


  • Antithyroid Agents
  • Methimazole
  • Propylthiouracil
  • Trinitrobenzenesulfonic Acid
  • Peroxidase