Hypergastrinemia increases proliferation of gastroduodenal epithelium during gastric ulcer healing in rats

Li, Hong; Helander, Herbert F.

doi:10.1007/bf02208582

Cited by 36 publications

(25 citation statements)

References 14 publications

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“…regenerative mucosa is increased in hypergastrinemic (19) and decreased in gastrin-depleted states (20). These studies have supported the concept that gastrin, whether triggered by endogenous mechanisms (i.e., omeprazole treatment) or exogenous hypergastrinemia (i.e., infusion of gastrin-17), stimulates cell proliferation in regenerative gastric mucosa (19).…”

mentioning

confidence: 54%

“…The growth-promoting effect of gastrin (18)(19)(20) has generated substantial interest because of potential side effects such as gastric or colorectal tumor growth during hypergastrinemia induced by long-term treatment with gastric acid-inhibitory drugs (38,39). The intra-…”

Section: Discussionmentioning

confidence: 99%

“…These studies have supported the concept that gastrin, whether triggered by endogenous mechanisms (i.e., omeprazole treatment) or exogenous hypergastrinemia (i.e., infusion of gastrin-17), stimulates cell proliferation in regenerative gastric mucosa (19). However, the molecular mechanisms that mediate these actions have not yet been identified or characterized, either in vitro or in vivo.…”

mentioning

confidence: 85%

“…To study the role of CCK receptors during wound healing, we selected a well-defined and established cryoulcer model in rats in which the in vivo effect of gastrin on regenerative mucosa can be quantified (3,4,19,20). This model has been extensively validated by evaluating a substantial number of various parameters, such as the expression of growth factors and their receptors, enzymes, and secretory products (2-6, 19, 20, 26-28).…”

mentioning

confidence: 99%

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Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

Schmassmann¹,

Reubi²

2000

J. Clin. Invest.

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mentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 85%

mentioning

confidence: 99%

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Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

Schmassmann¹,

Reubi²

2000

J. Clin. Invest.

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“…Using NIS-Elements BR (Nikon) software, a 100 -300 μm-wide area was outlined perpendicular to the mucosa and comprising the entire thickness of the mucosa. Within this area, all labelled and unlabelled epithelial cells/nuclei were counted [44] [45]. This procedure was repeated one to four times per rat.…”

Section: Immunohistochemistry Caspase 3 and Ki67mentioning

confidence: 99%

Histopathological Investigation of the Stomach of Rats Fed a 60% Genetically Modified Corn Diet

Zdziarski¹,

Carman²,

Edwards³

2018

FNS

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Genetic modification (GM) represents new opportunities for enhanced crop features such as improved insect resistance and herbicide tolerance. The technology allows for cross-species alterations, therefore potentially allowing a vast array of novel traits. Many GM crops have been developed and approved for human and animal consumption. The present study investigated a triple-stacked GM corn variety containing modifications for insect resistance (via cry1Ab and cry3Bb1 genes) and herbicide tolerance (via an EPSPS gene), which was fed to rats for six months. The study investigated the mucosa of the stomach. Alterations to tight junction apposition, gland dilatations with epithelial elongation and dysplasia in the GM-fed rats were observed. These results indicate that GM-corn may have an effect on rat stomach mucosa, which may have health implications.

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Classic NSAID and selective cyclooxygenase (COX)‐1 and COX‐2 inhibitors in healing of chronic gastric ulcers

Brzozowski¹,

Konturek

Konturek³

et al. 2001

Microscopy Res & Technique

135

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Prostaglandins (PG) derived from COX-1 are essential for the maintenance of mucosal integrity but COX-2 isoform synthesizes PG at a site of inflammation. Recently, COX-2 mRNA expression was demonstrated at the ulcer edge during healing of chronic gastric ulcers but the role for expression of COX-2 and its products such as PGE(2) and cytokines including interleukin (IL-1beta) and tumor necrosis factor alpha (TNFalpha) in ulcer healing remains unknown. In this study, Wistar rats with gastric ulcers produced by serosal application of acetic acid (ulcer area 28 mm(2)) received daily treatment either with: (1) vehicle (saline); (2) NS-398 (10 mg/kg-d i.g.) and Vioxx (5 mg/kg-d i.g.), both, highly specific COX-2 inhibitors; (3) meloxicam (5 mg/kg-d i.g.), a preferential inhibitor of COX-2; (4) resveratrol (10 mg/kg-d i.g.), a specific COX-1 inhibitor; (5) indomethacin (5 mg/kg-d i.g); and (6) aspirin (ASA; 50 mg/kg-d i.g.), non-selective inhibitors of both COX-1 and COX-2. At day 3, 7, and 14 after ulcer induction, the animals were sacrificed and the area of gastric ulcers was determined by planimetry and histology, gastric blood flow (GBF) at ulcer base and margin was measured by H(2) clearance technique, and blood was withdrawn for measurement of plasma IL-1beta and TNFalpha levels. The mucosal biopsy samples were taken for the determination of PGE(2) generation by RIA and expression of COX-1, COX-2, IL-1beta, and TNFalpha mRNA by RT-PCR. In vehicle-treated rats, gastric ulcers healed progressively and at day 14 the healing was completed, accompanied by a significant rise in the GBF at ulcer margin. The IL-1beta, TNFalpha, and COX-1 mRNA were detected in intact and ulcerated gastric mucosa, whereas COX-2 mRNA were upregulated only in ulcerated mucosa with peak observed at day 3 after ulcer induction. The plasma IL-1beta level was significantly increased at day 3 and 7 but then declined at day 14 to that measured in vehicle-controls. Indomethacin and ASA, which suppressed PGE(2) generation both in the non-ulcerated and ulcerated gastric mucosa, significantly delayed the rate of ulcer healing and this was accompanied by the fall in GBF at ulcer margin and further elevation of plasma IL-1beta and TNFalpha levels, which was sustained up to the end of the study. Treatment with NS-398 and Vioxx, which caused only a moderate decrease in the PGE(2) generation in the non-ulcerated gastric mucosa, delayed ulcer healing and attenuated significantly the GBF at ulcer margin and PGE(2) generation in the ulcerated tissue, while raising the plasma IL-1beta and TNFalpha similarly to those observed in indomethacin- and ASA-treated rats. Resveratrol, which suppressed the PGE(2) generation in both non-ulcerated and ulcerated gastric mucosa, prolonged ulcer healing and this was accompanied by the fall in the GBF at the ulcer margin and a significant increase in plasma IL-1beta and TNFalpha levels. We conclude that (1) classic NSAID delay ulcer healing due to suppression of endogenous PG, impairment in GBF at ulcer area, and excessive cyt...

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Hypergastrinemia increases proliferation of gastroduodenal epithelium during gastric ulcer healing in rats

Cited by 36 publications

References 14 publications

Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

Histopathological Investigation of the Stomach of Rats Fed a 60% Genetically Modified Corn Diet

Classic NSAID and selective cyclooxygenase (COX)‐1 and COX‐2 inhibitors in healing of chronic gastric ulcers

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