Effect of sialoadenectomy on ethanol-induced gastric mucosal damage in the rat: role of neutrophils

1990 ◽  
Vol 68 (2) ◽  
pp. 207-210 ◽  
Author(s):  
B. L. Tepperman ◽  
B. D. Soper
Keyword(s):  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Salivary Glands ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Mucosal Inflammation ◽  
Prostaglandin E ◽  
Epidermal Growth ◽  
Extent Of Damage

We have observed that removal of the salivary glands is associated with an increase in the susceptibility to gastric mucosal damage in the rat. In the present study, we have examined the effect of sialoadenectomy on ethanol-induced mucosal hemorrhagic damage and myeloperoxidase (MPO) activity. Hemorrhagic damage and MPO activity in response to intragastric 50% w/v ethanol were greater in sialoadenectomized rats when compared with sham-operated animals. Pretreatment with 16,16-dimethylprostaglandin E2 (0.3 μg/kg s.c.) reduced damage and MPO activity in both sialoadenectomized and sham control rats receiving 50% ethanol. The reduction in these parameters was greater in control than in sialoadenectomized rats. Pretreatment with epidermal growth factor (5 μg/kg s.c.) significantly reduced MPO activity but did not significantly affect the extent of damage. These data suggest that sialoadenectomy is associated with an increase in mucosal inflammation in animals given ethanol. However, in some situations tissue inflammation (as indicated by MPO activity) was reduced, while the proportion of gastric mucosa exhibiting hemorrhagic damage was not changed.Key words: salivary glands, gastric mucosa, neutrophils, prostaglandin E2, epidermal growth factor.

The effect of sialoadenectomy on gastric mucosal integrity in the rat: roles of epidermal growth factor and prostaglandin E2

1989 ◽  
Vol 67 (12) ◽  
pp. 1512-1519 ◽  
Author(s):  
B. L. Tepperman ◽  
J. A. Kiernan ◽  
B. D. Soper
Keyword(s):  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Salivary Glands ◽  
Ethanol Administration ◽  
Prostaglandin E ◽  
Functional Link ◽  
Mucosal Integrity ◽  
Epidermal Growth ◽  
And Control

Removal of the salivary glands (SALX) in rats has been shown to increase the susceptibility of gastric mucosa to ulcerogens. In the present study, we have investigated the role of specific salivary glands in this response. In addition, we have examined whether a functional link exists between the salivary glands, epidermal growth factor (EGF), and prostaglandin E2 (PGE2) by determining whether SALX decreases the responsiveness of the mucosa to the protective actions of either of both of these agents. Removal of the parotid salivary glands did not significantly increase ulceration in response to intragastric administration of 100% w/v ethanol. Animals were examined 60 min after ethanol administration. Removal of the submandibular–sublingual gland complexes was associated with a significant increase in the area of mucosal damage and a decrease in gastric pit depth in ethanol-treated animals when compared with sham-operated control rats. Furthermore, in both SALX and control animals, exogenous PGE2 and EGF resulted in a dose-dependent reduction in both groups of animals, although the protective effects of PGE2 and EGF were attenuated in SALX rats. PGE2 and EGF administered in combination resulted in the same degree of protection in both SALX and control rats. Sialoadenectomy resulted in a reduction in mucosal PGE2 synthesis. EGF administration did not consistently increase mucosal PGE2 synthesis. Conversely, sialoadenectomy did not reduce mucosal levels of EGF nor did exogenous PGE2 consistently increase salivary or mucosal content of EGF. If animals were examined 5 min after ethanol instillation, there were no differences in the degree of damage between SALX and control animals whether determined by measuring surface areas of lesions or changes in histology. These data suggest that SALX is associated with a reduction in the responsiveness of rat gastric mucosa to PGE2 and EGF. The data is not totally consistent with reductions in endogenous levels or synthesis of these agents.Key words: salivary glands, mucosal integrity, EGF immunoassay, PGE2 synthesis.

Aging: altered responsiveness of gastric mucosa to epidermal growth factor

1989 ◽  
Vol 257 (4) ◽  
pp. G554-G560 ◽  
Author(s):  
A. P. Majumdar ◽  
F. L. Arlow
Keyword(s):  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Membrane Fraction ◽  
Kinase Activity ◽  
Thymidine Kinase Activity ◽  
Epidermal Growth ◽  
K Activity

The present investigation examines the responsiveness of the gastric mucosa to the growth-promoting action of epidermal growth factor (EGF) during advancing age. Two sets of experiments were performed. In the first set of experiments, groups of 4-, 8-, 16-, and 24-mo-old Fischer 344 rats were injected subcutaneously at 12-h intervals for 2 days with either EGF (10 micrograms/kg) in gelatin or the vehicle only (controls). The animals were killed 16-18 h after the last injection. The oxyntic gland mucosa was assayed for thymidine kinase and the rate of DNA synthesis in vitro (indicators of proliferative activity) as well as for tyrosine kinase (Tyr-k) activity. In control rats, the rate of DNA synthesis and thymidine kinase activity rose steadily between 4 and 24 mo of age. However, whereas Tyr-k activity in the gastric mucosal cytosol changed only marginally with age, activity of the enzyme in the membrane fraction rose steadily between 4 and 16 mo and then increased abruptly. EGF stimulated gastric mucosal DNA synthesis and thymidine kinase activity in 4- to 16-mo-old rats compared with the corresponding controls, but in the 24-mo-old animals, it caused a significant 40-50% inhibition. EGF had no demonstrable effect on Tyr-k activity in either cytosolic or membrane fraction. We postulated that Tyr-k activity might have returned to basal level 16-18 h after the last EGF injection.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Protective Effect of Ocotillol, the Derivate of Ocotillol-Type Saponins in Panax Genus, against Acetic Acid-Induced Gastric Ulcer in Rats Based on Untargeted Metabolomics

2020 ◽  
Vol 21 (7) ◽  
pp. 2577 ◽  
Author(s):  
Cuizhu Wang ◽  
Yuze Yuan ◽  
He Pan ◽  
Alan Chen-Yu Hsu ◽  
Jinluan Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acetic Acid ◽  
Gastric Ulcer ◽  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Serum Levels ◽  
Gastroprotective Effect ◽  
Epidermal Growth ◽  
Oxide Synthase

Gastric ulcer (GU), a prevalent digestive disease, has a high incidence and is seriously harmful to human health. Finding a natural drug with a gastroprotective effect is needed. Ocotillol, the derivate of ocotillol-type saponins in the Panax genus, possesses good anti-inflammatory activity. The study aimed to investigate the gastroprotective effect of ocotillol on acetic acid-induced GU rats. The serum levels of endothelin-1 (ET-1) and nitric oxide (NO), the gastric mucosa levels of epidermal growth factor, superoxide dismutase and NO were assessed. Hematoxylin and eosin staining of gastric mucosa for pathological changes and immunohistochemical staining of ET-1, epidermal growth factor receptors and inducible nitric oxide synthase were evaluated. A UPLC-QTOF-MS-based serum metabolomics approach was applied to explore the latent mechanism. A total of 21 potential metabolites involved in 7 metabolic pathways were identified. The study helps us to understand the pathogenesis of GU and to provide a potential natural anti-ulcer agent.

scholarly journals Role of capsaicin sensitive nerves in epidermal growth factor effects on gastric mucosal injury and blood flow

Gut ◽  
1998 ◽  
Vol 42 (3) ◽  
pp. 344-350 ◽  
Author(s):  
J Y Kang ◽  
C H Teng ◽  
F C Chen ◽  
A Wee
Keyword(s):  
Blood Flow ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
Gastric Mucosal Damage ◽  
Arterial Infusion ◽  
Epidermal Growth

Background—Epidermal growth factor (EGF) and capsaicin protect against experimental gastric mucosal injury. Capsaicin exerts its gastroprotective effect by stimulating afferent neurones leading to release of calcitonin gene related peptide (CGRP) which causes gastric hyperaemia. EGF also causes gastric hyperaemia but whether it acts via capsaicin sensitive neurones is unknown.Aims—To assess the influence of: (1) capsaicin desensitisation on EGF effects on gastric mucosal injury and gastric mucosal blood flow; and (2) close arterial infusion of hCGRP8–37, a CGRP antagonist, on EGF effects on gastric mucosal blood flow.Methods—The absolute ethanol induced gastric mucosal injury model in the rat was used. Gastric mucosal damage was assessed by planimetry and light microscopy. Gastric mucosal blood flow was measured by laser Doppler flowmetry in a gastric chamber preparation.Results—Capsaicin desensitisation abolished the gastroprotective and gastric hyperaemic effects of EGF. Close arterial infusion of hCGRP8–37 antagonised the hyperaemic effect of both capsaicin and EGF.Conclusion—Results show that EGF may exert its gastroprotective and gastric hyperaemic effects via capsaicin sensitive afferent neurones.

Epidermal Growth Factor Induces Cell Proliferation in Mouse Pancreas and Salivary Glands

Pancreas ◽  
1997 ◽  
Vol 14 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Bodil Ohlsson ◽  
Claes Jansen ◽  
Ingemar Ihse ◽  
Jan Axelson
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Salivary Glands ◽  
Mouse Pancreas ◽  
Epidermal Growth

scholarly journals Growth Hormone and Epidermal Growth Factor in Salivary Glands of Giant and Dwarf Transgenic Mice

2004 ◽  
Vol 52 (9) ◽  
pp. 1191-1197 ◽  
Author(s):  
William G. Young ◽  
German O. Ramirez-Yañez ◽  
Terry J. Daley ◽  
Joseph R. Smid ◽  
Karen T. Coshigano ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Transgenic Mice ◽  
Salivary Glands ◽  
Epidermal Growth
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