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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Cell proliferation of the rat gastrointestinal mucosa after treatment with E2 prostaglandins and indomethacin.

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 X kg-1, b.d.), 15-R-15 methyl prostaglandin E2 (2 mg X kg-1, b.d.) or indomethacin (1.0-3.0 mg X 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.[1]


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