title: Association of maternal pancreatic function and foetal growth in rats treated with DFU, a selective cyclooxygenase-2 inhibitor.
abstract: Constitutive (COX-1) and inducible (COX-2) cyclooxygenase isoforms have been detected in various mammalian tissues. Their activity is blocked by non-steroidal anti-inflammatory drugs that may induce various side reactions. The aim of the study was to evaluate the effects of DFU, a selective COX-2 inhibitor, on exocrine and endocrine pancreatic function and the immunoexpression of both COX isoforms in maternal and foetal rat pancreases. The compound was administered to pregnant Wistar rats once daily from the 8th to the 21st day of gestation. Glucose level and amylase activity were determined in the maternal sera. Maternal and foetal pancreases were examined histologically. Immunoexpression of COX-1 and COX-2 was also evaluated. Both biochemical parameters, as well as the histological structure of the pancreas were undisturbed in the dams and their foetuses. The maternal glucose level was found to be an important factor for foetal growth. Strong cytoplasmic COX-1 immunostaining was observed in acinar secretory cells, whereas in islets the immune reaction was weak. Endocrine cells also revealed strong cytoplasmic COX-2 staining in the maternal and foetal pancreases. Acinar cells exhibited nuclear reaction, which was strong in the foetal but weak in the maternal pancreases. No differences in COX immunoexpression were found between the DFU-exposed and the control groups in either mothers or foetuses. It should be stressed that DFU administered throughout mid and late pregnancy in rats did not change maternal or foetal pancreatic morphology or immunoexpression of either of the main COX isoforms in the organ.
authors.affiliation: Experimental Teratology Unit of the Human Anatomy Department, Medical University of Lublin, Poland. fb3@wp.pl
authors.forename: F
authors.initials: F
authors.lastname: Burdan
authors.forename: J
authors.initials: J
authors.lastname: Szumiło
authors.forename: J
authors.initials: J
authors.lastname: Dudka
authors.forename: M
authors.initials: M
authors.lastname: Szumiło
authors.forename: A
authors.initials: A
authors.lastname: Korobowicz
authors.forename: S
authors.initials: S
authors.lastname: Chatterjee
authors.forename: R
authors.initials: R
authors.lastname: Klepacz
mesh_terms: D000681:Amylases / Q000378:metabolism; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D051545:Cyclooxygenase 1 / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D005260:Female; D047109:Fetal Development / Q000187:drug effects / Q000502:physiology*; D005663:Furans / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D010179:Pancreas / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar
chemical_list: C106876:5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanone; D052246:Cyclooxygenase 2 Inhibitors; D005663:Furans; D007527:Isoenzymes; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D000681:Amylases; D005947:Glucose