Role of cyclooxygenase-2 in modulating gastric acid secretion in the normal and inflamed rat stomach

2000 ◽  
Vol 279 (6) ◽  
pp. G1292-G1297 ◽  
Author(s):  
Kirsty Barnett ◽  
Cameron J. Bell ◽  
Webb McKnight ◽  
Michael Dicay ◽  
Keith A. Sharkey ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Ulcer Healing ◽  
Cyclooxygenase 2 ◽  
Gastric Ulcer Healing ◽  
Cyclooxygenase 1 ◽  
Basal Acid ◽  
Inflammatory Drugs

Nonsteroidal anti-inflammatory drugs elevate gastric acid secretion, possibly contributing to their ability to interfere with gastric ulcer healing. Inhibitors of cyclooxygenase-2 have been shown to delay experimental gastric ulcer healing. In the present study, we tested the hypothesis that cyclooxygenase-2-derived prostaglandins modulate gastric acid secretion. Studies were performed in normal rats and in rats with iodoacetamide-induced gastritis. Inflammation in the latter group was confirmed histologically and by a threefold increase in tissue levels of the granulocyte marker myeloperoxidase and was also associated with overexpression of cyclooxygenase-2 in the stomach. Basal acid secretion in both groups of rats was not affected by pretreatment with DuP-697, a selective inhibitor of cyclooxygenase-2. A nonselective cyclooxygenase inhibitor, indomethacin, had no effect on acid secretion in normal rats but caused a doubling of acid secretion in the rats with gastritis. DuP-697 had no effect on pentagastrin-induced secretion in either group of rats. Gastritis itself was associated with significantly increased pentagastrin-induced acid secretion, and this was further increased in rats pretreated with indomethacin. These results suggest that in a setting of gastric inflammation, prostaglandins derived from cyclooxygenase-1, not cyclooxygenase-2, exert inhibitory effects on acid secretion.

scholarly journals Accelerated gastric ulcer healing in thyroxine-treated rats: roles of gastric acid, mucus, and inflammatory response

2018 ◽  
Vol 96 (6) ◽  
pp. 597-602 ◽  
Author(s):  
Olasupo S. Adeniyi ◽  
Benjamin O. Emikpe ◽  
Samuel B. Olaleye
Keyword(s):  
Gastric Ulcer ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Ulcer Healing ◽  
Gastric Mucus ◽  
Gastric Ulcer Healing ◽  
Neutrophil Lymphocyte Ratio ◽  
Ulcer Area ◽  
Thyroxine Treatment ◽  
Male Wistar Rats

The roles of gastric acid, mucus, and inflammation on the pro-ulcer-healing effect of thyroid hormone were investigated. Male Wistar rats were randomly divided into four groups: control, thyroidectomised, thyroidectomised with thyroxine treatment (100 μg·kg–1·day–1), and sham-operated animals treated with thyroxine. Thirty-five days after thyroidectomy, sham surgery, or thyroxine treatment, an ulcer was experimentally induced. Healing was assessed 3, 7, and 10 days post-ulceration by measurement of the ulcer area, gastric mucus and acid secretion, and neutrophil lymphocyte ratio (NLR) as an index of inflammation. By day 10, the ulcer area had decreased in all groups. Recovery was significantly greater (P < 0.05) in thyroxine-treated rats (78.5% ± 1.6% reduction in ulcer area) than in controls (72.3% ± 1.2% reduction) or thyroidectomised rats (63.3% ± 1.9% reduction). Thyroxine-treated animals also had the highest reduction in NLR (65.0% ± 2.5%). Mucus secretion was significantly lower (P < 0.05) in thyroidectomised rats by days 3 and 7. Furthermore, by day 10, the concentration of basal acid decreased by 77.4% ± 2.6% in thyroxine-treated, 65.0% ± 0.0% in control, and 51.5% ± 3.3% in thyroidectomised rats. We conclude that thyroxine accelerates gastric ulcer healing by altering mucus and acid secretion and reducing NLR.

Chronic gastric ulcer healing in rats subjected to selective and non-selective cyclooxygenase-2 inhibitors

2002 ◽  
Vol 442 (1-2) ◽  
pp. 125-135 ◽  
Author(s):  
Bettina Berenguer ◽  
Catalina Alarcón de la Lastra ◽  
Francisco Javier Moreno ◽  
Maria José Martı́n
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Cyclooxygenase 2 ◽  
Chronic Gastric Ulcer ◽  
Gastric Ulcer Healing ◽  
Cyclooxygenase 2 Inhibitors

Role of nuclear factor-κB in gastric ulcer healing in rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto
Keyword(s):  
Gastric Ulcer ◽  
Mrna Expression ◽  
Ulcer Healing ◽  
Nuclear Factor Κb ◽  
Normal Mucosa ◽  
Cyclooxygenase 2 ◽  
Interleukin 1Β ◽  
Nuclear Factor ◽  
Gastric Ulcer Healing

We investigated the role of nuclear factor-κB (NF-κB) in gastric ulcer healing in rats. NF-κB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-κB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1β activated NF-κB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-κB action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1β. Persistent prevention of NF-κB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1β, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-κB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.

scholarly journals Gastric acid secretion in cyclooxygenase-1 deficient mice

2000 ◽  
Vol 14 (10) ◽  
pp. 1365-1370 ◽  
Author(s):  
F. Borrelli ◽  
N. J. Welsh ◽  
G. Sigthorsson ◽  
R. Simpson ◽  
A. Palizban ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Cyclooxygenase 1 ◽  
Deficient Mice

The endoscopic studies on the gastric acid secretion (III) with relation to gastric ulcer

1966 ◽  
Vol 1 (4) ◽  
pp. 54-54
Author(s):  
N. Senda ◽  
H. Inui ◽  
S. Okuda ◽  
T. Itoh ◽  
T. Saegusa ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid

Impaired gastric acid secretion in mast cell-deficient mice

1990 ◽  
Vol 259 (1) ◽  
pp. G41-G47 ◽  
Author(s):  
D. J. Stechschulte ◽  
D. C. Morris ◽  
R. L. Jilka ◽  
D. J. Stechschulte ◽  
K. N. Dileepan
Keyword(s):  
Mast Cell ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Parietal Cells ◽  
Secretory Response ◽  
H2 Antagonist ◽  
Significant Difference ◽  
Basal Acid ◽  
Deficient Mice

Gastric acid secretion in normal (+/+) C57B1/6J mice and congeneic, mast cell-deficient (mi/mi) C57B1/6J mice was examined. The mast cell-deficient animals had approximately 50% of the normal quantity of gastric histamine and a blunted basal acid level and secretory response. These observations were noted despite the presence of parietal cells, which were normal in number and morphology. The H2-antagonist ranitidine inhibited basal acid secretion in both groups of animals. Exogenous histamine induced a significant secretory response in normal and mast cell-deficient groups, but only the secretory response in normal animals could be blocked by the H2-antagonist. Treatment of mast cell-deficient animals with histamine for seven consecutive days before stimulation did not restore the histamine response to the normal (+/+) levels. The normal animals demonstrated an acid secretory response to pentagastrin. Mast cell-deficient mice also responded to pentagastrin, but the response was less than that observed in the normal animals, and a significant difference was not evident in all experiments. Furthermore, simultaneous injection of mast cell-deficient animals with histamine and pentagastrin did not restore pentagastrin responsiveness to normal levels, although the histamine concentration used was sufficient to raise acid secretion to basal levels of normal mice. These results support the conclusion that non-mast cell histamine only partially contributes to basal gastric acid secretion and is insufficient to facilitate full parietal cell responsiveness. Furthermore, pentagastrin requires the presence of mast cells to elicit a maximal secretory response but can use non-mast cell histamine to activate the parietal cells for acid secretion.

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