Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

Glucocorticoids take part in the intense morphofunctional modifications tha t occur in the gastric mucosa during fetal and postnatal development. Two s tudies were designed to evaluate corticoids role in gastric cell proliferat ion and apoptosis in developing rats: in vivo, using suckling animals; in v itro, using gastric explants obtained from 20-day fetuses. These explants w ere cultured in DMEM/F12 medium treated or not with 50 ng/ml of corticoster one; after 22 hr, vincristine was added to the medium for 2 hr to block mit osis. The metaphasic index decreased significantly after the 24-hr treatmen t (controls: 1.52 +/- 0.53; treated: 0.40 +/- 0.21) and apoptotic cells wer e visualized under light and electron microscopy. Fifteen-day-old rats were treated with hydrocortisone (25 mg/Kg) for 3 days, and injected with BrDU (100 mg/Kg) 1 hr before sacrifice on the 18(th) day. BrDu-labeled and non-l abeled cells were counted to determine the labeling index of epithelial cel ls. As apoptotic cells are rapidly eliminated, other animals were treated f or only 2-3 hr. Sections were investigated for the presence of apoptotic ce lls, using morphological criteria and TUNEL labeling. Hydrocortisone signif icantly reduced the labeling index (controls: 15.6 +/- 1.6 vs. treated: 11. 7 +/- 1.1), besides altering the body weight gain. Hydrocortisone treatment doubled the number of apoptotic cells after 2 hr, and quadruplicated it af ter 3 hr. The results demonstrated that glucocorticoids inhibit cell prolif eration in the gastric epithelium of fetuses and suckling rats and increase apoptotic rates, suggesting the exit from cell cycle. Anat Rec 260: 213-22 1, 2000. (C) 2000 Wiley-Liss, Inc.