Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.20 (alpha-glucosidase)
 4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, the protective effect of PGE2 on intestinal damage in indomethacin-treated adult rats was investigated. Ileal integrity was evaluated making use of different biochemical and histological parameters: activities of sucrase, maltase and diamine oxidase; concentrations of DNA, putrescine, spermidine and spermine; incorporation of 3H-thymidine into DNA; mitotic index and mucosal thickness. Results expressed per g of mucosal weight, showed that: maltase and diamine oxidase activities as well as DNA, spermidine and spermine concentrations decreased markedly in indomethacin-treated rats when compared to control rats; the decrease of maltase activity as well as DNA, spermidine and spermine concentration was less pronounced in PGE2-treated rats when compared to indomethacin-treated rats; 3H-thymidine incorporation into DNA and mitotic index values showed no significant variation in the course of different treatments; mucosal thickness increased strongly, in PGE2-protected rats. We suggest that PGE2 could protect the rat's intestinal mucosa against the effects of indomethacin through a trophic action on intestinal villi.
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PMID:Effect of prostaglandin E2 on the small intestine of indomethacin-treated rats. 311 78

Exogenous 16,16-di-methyl-prostaglandin (PG) E2 administration augments mucosal hyperplasia after massive small bowel resection in the rat. We, therefore, evaluated the ability of aspirin to inhibit mucosal PG synthesis in the small intestine and further evaluated the effects of reduced PG synthesis on mucosal adaptation after a 70% jejunoileal resection in male Sprague-Dawley rats. Sixteen of 27 resected and 8 of 16 sham-operated rats were given aspirin 20 mg/kg body wt subcutaneously every 8 h for 12 days; the remainder were given vehicle only. Although mucosal PGE2, PGF2 alpha, and thromboxane B2 synthesis were all reduced by aspirin administration to 20-40% of the control values, mucosal adaptation in resected animals as measured by mucosal weight, DNA, protein, and maltase levels was only inhibited in the distal ileum. Aspirin did not affect these values in the duodenum, the upper jejunum, and the midileum. This study provides evidence for some involvement of endogenous PGs in regulation of the mucosal adaptation process in the distal ileum after massive small bowel resection in the rat. However, lack of inhibition more proximally suggests that factors other than PGs are more important.
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PMID:Reduced mucosal prostaglandin synthesis after massive small bowel resection. 327 15

Prostaglandins have been reported to exert trophic effects on gastrointestinal tissues. To determine whether there is a direct interaction with enterocytes, prostaglandins PGE2, PGF2 alpha, PGA2, PGB2 and the stable PGE2 derivative suleprost as well as the prostacyclin derivative nileprost were tested in rabbit ileal mucosa under organ culture conditions. At concentrations between 10(-9) and 10(-5) M, none of the prostaglandins significantly affected biopsy DNA or protein content, or the activity of the brush border enzymes alkaline phosphatase, lactase, sucrase or maltase. The inhibition of endogenous prostaglandin synthesis with indomethacin also failed to alter these parameters. Moreover, the growth rate of a rat duodenal crypt cell line was unaffected when cultured in the presence of PGE2, PGF2 alpha or indomethacin. Thus, there was no evidence for a direct effect of exogenous or endogenous prostaglandins or their deficiency on the differentiation or growth in cultured small intestinal cells.
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PMID:Prostaglandins are not involved in the differentiation or growth of cultured small intestinal cells. 381 31

Several markers of growth and biochemical development in the rat were studied after administration of prostacyclin (PGI2) and 16, 16-dimethyl prostaglandin E2 (16, 16DM PGE2). Intermittent administration of PGI2 for 3 days to 10- and 19-day-old animals, with subsequent sacrifice at 14 and 23 days, resulted in significant dose related decreases in growth at 23 days. Total sucrase and maltase (glucoamylase) activities were elevated compared to controls at 14 days. Total activities of these enzymes were decreased in postweaned 23-day-old animals, but specific activities per mg intestinal protein were not significantly different. 16, 16DM PGE2 administered continuously between day 10-16 of life caused alterations in growth as well as increases in sucrase and maltase (glucoamylase) activities. Exogenously administered prostaglandins, therefore, are associated with altered growth and markers of biochemical development in the rat.
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PMID:Prostaglandin-mediated effects on growth and markers of biochemical development in the rat. 641 40

The effect of repeated oral administration of prostaglandin analogue (dmPGE2) on intestinal macromolecular transport and digestive enzymes development were investigated in the suckling rats. By the administration of dmPGE2 for 7 days, precocious induction of maltase activity, depression of amylase activity and enhancement of trypsin activity in the pancreas occurred. Absorption of bovine IgG was dose dependently depressed by dmPGE2 treatments. The intestinal cessation was also observed in the adrenalectomized pups, but was not influenced by difluoromethyl ornithine administration. These results suggest that oral administration of PGE2 induces precocious maturation of the small intestine and exocrine pancreas and that the intestinal cessation is not directly related to ornithine decarboxylase activity in the suckling rats.
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PMID:Precocious cessation of intestinal macromolecular transport and digestive enzymes development by prostaglandin E2 in suckling rats. 752 52