Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Investigation about the histamine receptors of gastric smooth muscle cells was done using isolated gastric smooth muscle cells of guinea pig. Isolated gastric smooth muscle cells were prepared from the stomach of guinea pig by percoll density gradient centrifugation after enzymatic digestion with collagenase and dyspase. Contraction of the cells was determined by image of phase-contrast microscopy and digitizer and expressed as the mean per cent of control in cell axis length. The concentration of intracellular Ca2+ ([Ca2+]i) was measured with the calcium-sensitive dye fura-2. Tested drugs were added to the incubation medium containing 2 mM CaCl2. Both contractile response and [Ca2+]i increased following histamine stimulation in a dose-dependent manner from 10(-7) to 10(-4) M, and those peaks were obtained in application of 10(-4) M pyridylethylamine, a H1 receptor agonist, made an increase in [Ca2+]i as much as 10(-4) M histamine. But 10(-4) M dymaprit, a H2 receptor agonist, made only small increase in [Ca2+]i, whose value was similar to that in application of only 2 mM CaCl2. 10(-4) M pyrilamine, a H1 receptor antagonist, inhibited the response to 10(-4) M histamine, and the value was similar to that in application of only 2 mM CaCl2. Cimetidine, a H2 receptor antagonist, did not inhibit the response to 10(-4) M histamine stimulation at all. From those results it is concluded that the action of histamine to the gastric smooth muscle cells of guinea pig may be mediated through H1 receptor, but not through H2 receptor.
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PMID:[Studies on the contractile mechanism of isolated gastric smooth muscle cells of guinea pig--investigation of the histamine receptor]. 198 90

The healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin were investigated with reference to the enzyme activity of both prolylhydroxylase and collagenase as related to histological findings. The rats were observed by endoscopy on the 3rd day after the subserosal injection of acetic acid; rats with ulcers were divided into three groups: non-treated, and cimetidine- and calcitonin-treated. The latter two groups were treated for 7 days. Prolylhydroxylase activity in active ulcers in the non-treated group was slightly higher on the 3rd day and significantly higher on the 10th day than the activity in control rats that had received subserosal injections of physiological saline solution on the respective days. In non-treated rats, the healed ulcer on the 10th day showed lower prolylhydroxylase activity than that in the active ulcer on the same day. Cimetidine did not affect prolylhydroxylase activity, but, with calcitonin, there was higher prolylhydroxylase activity in the healed than in the active ulcer, although the difference was not significant. Interstitial collagenase showed the highest activity on the 3rd day and decreased on the 10th day in non-treated rats. Collagenase activity was higher in the cimetidine-treated group, than that in the non-treated group, and numerous peroxidase-positive granulocytes were seen in the mucosa and submucosa. Calcitonin did not affect collagenase activity. The participation of both enzymes is indispensable in the healing process and the effects of anti-ulcer agents on these enzymes must be considered.
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PMID:Wound healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin, with special reference to prolylhydroxylase and collagenase enzyme activity. 764 95

The effects of aspirin and ibuprofen on pepsinogen secretion were studied in isolated human peptic cells prepared from endoscopically obtained biopsy specimens after collagenase digestion, mechanical disruption, and percoll gradient centrifugation. Pharmacological concentrations of aspirin and ibuprofen (10(-8)-10(-4) M), potentiated histamine (10(-6)-10(-4)M) and forskolin (10(-5)M) stimulated pepsinogen secretion without affecting basal secretion, acetylcholine (10(-6)M) stimulated pepsinogen secretion or cell vitality. Augmentation of secretagogue stimulated pepsinogen secretion was dependent on extracellular calcium because potentiation was abolished by calcium depletion of the medium. Cimetidine inhibited the potentiation effect on histamine but not on forskolin stimulated pepsinogen secretion, thus suggesting that this augmentation was independent of histamine H2 receptors. Of interest, potentiation was also independent of endogenous prostaglandin inhibition because exogenous addition of prostaglandin E2 and D2 increased both basal and acetylcholine stimulated pepsinogen secretion in a dose dependent way, but they did not modify histamine or histamine plus aspirin or ibuprofen stimulated pepsinogen secretion. In conclusion, aspirin and ibuprofen potentiate secretagogue stimulated pepsinogen secretion by dispersed human peptic cells and this might be an additional mechanism of non-steroidal anti-inflammatory drug (NSAID) induced gastric injury. This potentiation effect is regulated by calcium, independent of endogenous prostaglandin inhibition and seems to act on pepsinogen secretion at a post-receptor site.
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PMID:Non-steroidal anti-inflammatory drugs and prostaglandin effects on pepsinogen secretion by dispersed human peptic cells. 779 13