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PubMed1981

Effects of inflammatory agents on endothelial lysosomal fragility and their inhibition by anti-inflammatory drugs.

1. Endothelial cells from human umbilical veins were maintained in tissue culture. The fragility of lysosomal membranes were studied by microdensitometry. 2. Histamine (50 microM to 10 mM), 4-methylhistamine (100 nM to 10 mM) and dimaprit (100 nM to 10 mM) increased lysosomal fragility. 2-Thiazolylethylamine and 2-pyridylethylamine (100 nM to 10 mM) had no effect. 3. Prostaglandins E1 and E2 (3 nM to 30 microM) and prostaglandin F2 alpha (2 nM to 20 microM) had no direct effect. Low concentrations of prostaglandins E1 and E2 inhibited the fragility induced by histamine 100 microM. 4. Bradykinin (100 nM to 100 microM) decreased fragility. 5. The increase in fragility induced by histamine 100 microM or dimaprit 100 microM was inhibited by cimetidine (100 microM to 1 mM) but not by mepyramine (1 microM to 1 mM). 6. Pretreatment with indomethacin, hydrocortisone, ibuprofen and sodium salicylate caused a dose-dependent inhibition of histamine-induced fragility. Threshold concentrations were 1 pM, 100 pM, 10 nM and 10 microM, respectively. 7. Lignocaine (1 microM to 1 mM) had no direct effect and did not decrease histamine-induced fragility.

Anti-Inflammatory Agents↗
PubMed1992

Studies of gut mucosal protein synthesis in a non-steroidal anti-inflammatory drug (NSAID) model of inflammatory bowel disease.

The extent to which defects in protein synthesis occurred in an experimental indomethacin induced rat model of nonsteroidal enteropathy has been examined. Male rats (nine) were fed indomethacin (8 mg/kg/day) for three days mixed with a powdered form of chow. The control group of rats (nine) were fed the same diet for three days without indomethacin. After the feeding period, both groups were fed a normal solid diet for four days. At the end of this period, the fractional rates of intestinal protein synthesis was determined by the 'flooding dose' technique. The mucosal protein, RNA and DNA contents in the proximal ileum of animals with enteropathy were not significantly different from controls (p greater than 0.05). Experimental enteropathy induced selective increases in the fractional rates of protein synthesis (26% increase, p less than 0.03) and RNA activities (23% increase, p less than 0.04). There were no significant changes in any of these variables in the duodenum (p greater than 0.05 in all instances). These changes may partly reflect the activity of those processes responsible for the pathogenic changes in NSAID enteropathy.

Animals↗