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Thickening of the glycocalyx during methotrexate induced small intestinal mucosal atrophy in the rat

H J Egberts1, J E van Dijk, J M Mouwen

  • 1State University of Utrecht, Department of Veterinary Pathology, The Netherlands.

Insights

Methotrexate (MTX) induced changes in rat small intestine glycocalyx. Villous enterocyte glycocalyx became more pronounced after MTX, with recovery by day six.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Histology

Background:

  • The small intestinal glycocalyx plays a crucial role in mucosal protection and nutrient absorption.
  • Understanding its response to injury is vital for treating gastrointestinal disorders.

Purpose of the Study:

  • To investigate the morphological changes in the small intestinal enterocyte glycocalyx following methotrexate-induced mucosal atrophy in rats.
  • To observe the temporal dynamics of these glycocalyx alterations.

Main Methods:

  • Wistar rats were administered intraperitoneal methotrexate (MTX) to induce mucosal atrophy.
  • Tissue specimens from the Treitz' ligament were collected on days 2, 4, and 6 post-injection.
  • Electron microscopy with osmium tetroxide and potassium ferrocyanide fixation was used to visualize glycoconjugates.

Main Results:

  • Control rats showed minimal glycocalyx on villous enterocytes but prominent glycocalyx on crypt enterocytes.
  • MTX administration led to a more pronounced villous enterocyte glycocalyx by day 2.
  • By day 4, significant microvilli shortening and pronounced glycocalyces were observed on villous enterocytes, while crypt cells maintained well-developed cell coats.
  • By day 6, the glycocalyx morphology in both villous and crypt cells approached normal levels.

Conclusions:

  • Methotrexate-induced mucosal atrophy causes significant, yet reversible, alterations in the small intestinal glycocalyx.
  • The villous enterocyte glycocalyx shows a notable increase in prominence following MTX treatment.
  • These findings highlight the dynamic nature of the glycocalyx in response to chemical injury.

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