Cell Proliferation of the Rat Gastrointestinal Mucosa after Treatment with E₂ Prostaglandins and Indomethacin

Abstract

The frequency of arrested mitoses after vincristine injection was studied in the gastrointestinal mucosa of rats treated with either natural prostaglandin E₂ (0.2–5.0 mg·kg^-1, b.d.), 15-R-15 methyl prostaglandin E₂ (2 mg•kg^-1, b.d.) or indomethacin (1.0–3.0 mg•kg^-1, b.d.). In addition to the mitotic index, morphometric measurements including the mucosal thickness and the thickness of the proliferative and functional zones of the gastric corpus, antrum and jejunum were performed. Natural prostaglandin E₂, at the highest dose range, reduced significantly the mitotic index in the gastric antrum. Normal values were found in the gastric corpus and jejunum and in the antrum with the lower doses. The mitotic index was unaffected by treatment with 15-R-15 methyl prostaglandin E₂. Natural prostaglandin E₂ produced trophic changes (i.e. increased thickness and/or hyperplasia) in the antrum, functional epithelial zone of the gastric corpus and in the jejunum. More pronounced trophic changes were observed in the mucosa of rats treated with the analogue. Indomethacin reduced the mucosal thickness in all examined epithelia and lowered the mitotic index in the jejunum. It is concluded that the trophic effects of E₂ prostaglandins on gastrointestinal epithelia are not caused by increased production of new cells. The reduced mitotic index observed in the antral mucosa of prostaglandin-treated rats could be secondary to a negative feedback from the hyperplastic epithelium. The antitrophic effects of the prostaglandin-synthesis blocker (indomethacin) indicates that endogenous prostaglandins may participate in the epithelial cell regulation of the gastrointestinal tract.

Ventromedial hypothalamus lesions induce jejunal epithelial cell hyperplasia through an increase in gene expression of cyclooxygenase

“…[17][18][19] Moreover, we evaluated mRNA levels of cyclooxygenase (COX), a rate-limiting enzyme for prostaglandin (PG) synthesis, since PGs are also known to induce cell hyperplasia in the small intestine. 20,21 Materials and methods…”

Crypt stem cell survival in the mouse intestinal epithelium is regulated by prostaglandins synthesized through cyclooxygenase-1.

“…Exogenous PGE 2 produces epithelial hyperplasia in the intestine; the initial kinetic change is a reduction in epithelial cell loss from the villi (18). Inhibition of the synthesis of endogenous prostaglandins by nonsteroidal antiinflammatory drugs (NSAIDs) 1 was also associated with a decrease in cell proliferation.…”

Effects of extract F of red-rooted Salvia on mucosal lesions of gastric corpus and antrum induced by hemorrhagic shock-reperfusion in rats

“…In many physiological and pathophysiological conditions, PGI 2 has protective effect on gastric mucosa. On the contrary, TXA 2 may aggravate the gastric mucosal injury [38,39] . The present findings showed the PGE 2 and PGI 2 contents and PGI 2 /TXA 2 ratio in the antrum were markedly higher than those in the corpus after hemorrhagic shockreperfusion, showing gastric antrum was more resistant than gastric corpus.…”