Rat Stomach (rat + stomach)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


Immunocytochemical Detection of Synaptophysin in Enteric Neurones during Prenatal Development in the Rat Stomach

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2004
M. Asar
Summary In this study, the localization and appearance of synaptophysin-immunoreactive (IR) nerve cells and their relationships with the developing gastric layers were studied by immunocytochemistry and light microscopy in the embryonic rat stomach. The stomachs of Wistar rat embryos aged 13,21 days were used. The first neuronal bodies and their processes containing synaptophysin-immunoreactivity were observed on embryonic day 13. In contrast, synaptophysin-IR nerve terminals were first observed between mesenchymal cells on embryonic day 14. These results indicate that synaptophysin is expressed in growing neurits and neuronal cell bodies before these neurones have established synaptic connections. The occurrences of mesenchymal cell condensation near synaptophysin-IR neuroblasts on embryonic day 15 reflect an active nerve element-specific mesenchymal cell induction resulting in the morphogenesis of muscle cells. Similarly, the appearance of glandular structures after synaptophysin-IR neuroblasts, on embryonic day 18, suggests that the epithelial differentiation may be closely related to the neuronal maturation as well as other factors. Finally, synaptophysin is functionally important in neuronal development and maturation, together with the establishment of neuroneuronal and neuromuscular contacts and in epithelial differentiation. [source]


Effects of benzo[a]pyrene on tissue activities of metabolizing enzymes and antioxidant system in normal and protein-malnourished rats

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 2 2003
Osama A. Badary
Abstract The effects of benzo[a]pyrene (B[a]P) on some drug-metabolizing and antioxidant systems in liver, lung, and stomach were investigated in normal and protein malnutrition (PM) rats. PM significantly inhibited tissue glutathione (GSH) content and increased hepatic lipid peroxidation. Cytochrome P450 isoform CYP1A1 was significantly increased in various tissues (42,73%). Also, lung glutathione S-transferase (GST) activity was significantly decreased (19%) in PM rats. On the other hand, B[a]P significantly induced tissue GSH of control and PM rats. Also, hepatic lipid peroxidation were significantly increased in control rats treated with B[a]P. Superoxide dismutase (SOD) activity was decreased by B[a]P treatment in PM rat stomach. B[a]P significantly induced both quinone reductase (QR) (in all tissues) and hepatic GST of control and PM rats. GST activity in PM rat liver was significantly higher than that of control rat liver after B[a]P treatment. Also, B[a]P induced hepatic CYP1A1 by 32-fold and 27-fold (P , 0.05) in control and PM rats, respectively. Stomach and hepatic UDP-glucuronosyltransferase activities were significantly decreased (34%) and increased (74%), respectively by B[a]P in PM rats. The results suggest that PM status has a modifying effect on the response of some antioxidant and metabolizing systems to a well-known carcinogen risk. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:86,91, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10064 [source]


Influence of gender difference and gastritis on gastric ulcer formation in rats

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2001
Edgar SL Liu
Abstract Background: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. Methods: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E2 (PGE2) level were also determined. Results: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE2 level was higher in female rats with acute gastritis. Both mucus and PGE2 were increased during ulcer healing in both genders. Conclusions: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE2 not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach. [source]


The role of erythropoietin in the protection of gastric mucosa from indometacin-induced gastric injury and its relationship with oxidant and antioxidant parameters in rats

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2010
Fatih Albayrak
Abstract Objectives Erythropoietin has anti-oxidative and anti-inflammatory activity. We wanted to evaluate its activity in preventing damage to the gastric mucosa. Methods We examined the protective effect of erythropoietin on indometacin-induced gastric mucosa damage in the rat stomach and compared its potency with that of famotidine. We also measured effects on oxidant and antioxidant parameters in the rat stomach. Key findings Famotidine and erythropoietin 2500 and 5000 IU/kg reduced the ulcer area by 98%, 31% and 58%, respectively, compared with the indometacin group. Superoxide dismutase activity and glutathione level were decreased and myeloperoxidase activity increased in the indometacin group compared with healthy rats. Famotidine and erythropoietin at all doses increased superoxide dismutase and glutathione levels significantly compared with the indometacin group. Myeloperoxidase activity was decreased by erythropoietin and famotidine. Conclusions These results support the view that erythropoietin counteracts the effects of indometacin in inducing gastric ulcer and could be used as a an antiulcer compound. Its antiulcer effect is less potent than that of famotidine. The antiulcerogenic effects of erythropoietin may be related to its intrinsic ability to sustain the activities of free-radical scavenging enzymes and the bioavailability of glutathione. [source]


The roles of prostaglandin E receptor subtypes in the cytoprotective action of prostaglandin E2 in rat stomach

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000
H. Araki
Summary Aim: To investigate the EP receptor subtype involved in the gastroprotective action of prostaglandin (PG) E2 using various EP receptor agonists in rats, and using knockout mice lacking EP1 or EP3 receptors. Methods: Male SD rats and C57BL/6 mice were used after an 18-h fast. Gastric lesions were induced by oral administration of HCl/ethanol (150 m m HCl in 60% ethanol). Rats were given various EP agonists i.v. 10 min before HCl/ethanol: PGE2, sulprostone (EP1/EP3 agonist), butaprost (EP2 agonist), 17-phenyl-,-trinorPGE2 (17-phenylPGE2: EP1 agonist), ONO-NT012 (EP3 agonist) and 11-deoxyPGE1 (EP3/EP4 agonist). In a separate study, the effect of PGE2 on HCl/ethanol lesions was examined in EP1 - and EP3 -receptor knockout mice. Results: Gastric lesions induced by HCl/ethanol were dose dependently prevented by PGE2; this effect was mimicked by sulprostone and 17-phenylPGE2 and was significantly antagonized by ONO-AE-829, an EP1 antagonist. Neither butaprost, ONO-NT012 nor 11-deoxyPGE1 exhibited any protective activity against HCl/ethanol-induced gastric lesions. PGE2 caused an inhibition of gastric motility as well as an increase of mucosal blood flow and mucus secretion, the effects being mimicked by prostanoids activating EP1 receptors, EP2/EP3/EP4 receptors and EP4 receptors, respectively. On the other hand, although HCl/ethanol caused similar damage in both wild-type mice and knockout mice lacking EP1 or EP3 receptors, the cytoprotective action of PGE2 observed in wild-type and EP3 -receptor knockout mice totally disappeared in mice lacking EP1 receptors. Conclusion: The gastric cytoprotective action of PGE2 is mediated by activation of EP1 receptors. This effect may be functionally associated with inhibition of gastric motility but not with increased mucosal blood flow or mucus secretion. [source]


Interactive roles of endogenous prostaglandin and nitric oxide in regulation of acid secretion by damaged rat stomachs

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000
K. Takeuchi
Summary Background: The acid inhibitory mechanism in the damaged stomach is known to involve endogenous nitric oxide (NO) as well as prostaglandin (PG). Aim: To investigate the interaction between PG and NO in regulation of acid secretion in the stomach following damage. Methods: Under urethane anaesthesia, a rat stomach was mounted in an ex vivo chamber and perfused with saline. Acid secretion, luminal PGE2, NO metabolites (NOx) and histamine output were measured before and after application of 20 m m taurocholate Na (TC) for 30 min, with or without pre-treatment with indomethacin and/or NG -nitro- l -arginine methyl ester (L-NAME). Results: Exposure of the stomach to TC caused a decrease in acid secretion, with concomitant increase of both luminal NOx and PGE2. Either L-NAME or indomethacin reduced the decrease in acid secretion in response to TC, but only L-NAME allowed acid secretion to increase over basal values. L-NAME prevented the increase of luminal NOx after TC treatment, while indomethacin inhibited PGE2 release during and after exposure to TC. The increase in acid secretion in the presence of L-NAME was prevented when indomethacin was given concomitantly. TC treatment increased histamine output in the lumen, a process that was enhanced by L-NAME but reduced by indomethacin. Conclusions: Damage to the stomach increases both NO and PG in the lumen, and decreases acid secretion. Inhibiting NO production increases acid secretion in the damaged stomach, but only when PG biosynthesis is intact. It is assumed that endogenous PG has a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect probably through enhancing the release of mucosal histamine. [source]


Oxyntic lesions may be provoked in the rat both by the process of acid secretion and also by gastric acidity

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2000
Waldum
Background: Gastric ischaemia appears to be a common pathogenetic factor for stress ulcers. These ulcers occur predominantly in the oxyntic mucosa, suggesting that the acid secretory process or its stimulation is involved in the pathogenesis. Methods: We examined separately the role of the acid secretory process and gastric luminal acidity in the pathogenesis of gastric lesions using the isolated vascularly perfused acid-secreting rat stomach. Results: Pentagastrin-stimulated acid secretion induced submucosal bleeding in the oxyntic mucosa whether accompanied by perfusion of the gastric lumen with saline or a phosphate buffer at pH 7.0. On the other hand, acidity, whether endogenous or introduced by luminal perfusion, induced erosions in both the oxyntic and antral mucosa. Conclusion: It is concluded that the acid secretory process itself contributes to the particular vulnerability of the oxyntic mucosa to ischaemia. Histamine released upon stimulation of gastric acid secretion or shortage of energy due to the requirements for acid secretion may both contribute to this vulnerability. Furthermore, these findings suggest that inhibition of gastric acid secretion should be superior to antacids in preventing stress ulcers. [source]


Tension and stress in the rat and rabbit stomach are location- and direction-dependent

NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2005
J. Zhao
Abstract, Distension studies in the stomach are very common. It is assumed in pressure,volume (barostat) studies of tone and tension in the gastric fundus that the fundus is a sphere, i.e. that the tension in all directions is identical. However, the complex geometry of the stomach indicates a more complex mechanical behaviour. The aim of this study was to determine uniaxial stress,strain properties of gastric strips obtained from rats (n = 12) and rabbits (n = 10). Furthermore, we aimed to study the gastric zero-stress state since the stomach is one of the remaining parts of the gastrointestinal tract where residual strain studies have not been conducted. Longitudinal strips (in parallel with the lesser curvature) and circumferential strips (perpendicular to the lesser curvature) were cut from the gastric fundus (glandular part) and forestomach (non-glandular part). The residual stress was evaluated as bending angles (unit: degree per unit length and negative when bending outwards). The residual strain was computed from the change in length between the zero-stress state and no-load state. The stress,strain test was performed using a tensile test machine. The thickness and width of each strip were measured from digital images. The strips data were compared with data obtained in the intact stomach in vitro. Most residual stresses and strains were bigger in the glandular part than in the forestomach, and in general the rat stomach had higher values than the rabbit stomach. The glandular strips were stiffer than the forestomach strips and the longitudinal glandular strips were stiffer than the circumferential glandular strips (P < 0.05). The gastric strips were stiffer in rats than in rabbits (P < 0.01). The data obtained in the intact rat stomach confirmed the strips data and indicated that those were obtained in the physiological range. In conclusion, the biomechanical properties of the gastric strips from the rat and rabbit are location-dependent, direction-dependent and species-dependent. The assumption in physiological pressure,volume studies that the stomach is a sphere with uniform tension is not valid. Three-dimensional geometric data obtained using imaging technology and mechanical data are needed for evaluation of the stomach function. [source]


The Chinese herbal preparation Qing Yi Tang (QYT) improves intestinal myoelectrical activity and Increases intestinal transit during acute pancreatitis in Rodents

PHYTOTHERAPY RESEARCH, Issue 4 2007
Yong-Yu Li
Abstract The aim was to investigate alterations of intestinal motility in models of acute pancreatitis and to investigate the effects of the Chinese herbal preparation Qing Yi Tang (QYT) on these alterations. Upper gastrointestinal transit was evaluated in mice following induction of mild acute pancreatitis (MAP) using caerulein. Myoelectrical activity was recorded in rats after induction of severe acute pancreatitis (SAP) using sodium deoxycholate (SDOC). The contractility of jejunum segments was evaluated in the presence of SDOC, lipopolysaccharide (LPS) and trypsin. QYT accelerated the transit in MAP mice in a concentration dependent manner. Slow wave activity of smooth muscle in rat stomach and jejunum remained unchanged following SAP, but the spiking activity was significantly decreased, with bursts of 7.2 ± 2.6/10 min compared with 47.9 ± 13.2/10 min without SAP (p < 0.01). QYT reversed this decrease. Additionally, the amplitudes of slow waves and spikes were enhanced by QYT in SAP rats. The tension and amplitude of spontaneous contractile activity was reduced by SDOC and LPS and increased by trypsin. Gastrointestinal (GI) transit is altered by SAP but not by MAP. The Chinese herbal preparation QYT improves disturbed motility in AP by stimulating myoelectrical activity and accelerating GI transit. Copyright © 2007 John Wiley & Sons, Ltd. [source]


Immunocytochemical Detection of Synaptophysin in Enteric Neurones during Prenatal Development in the Rat Stomach

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2004
M. Asar
Summary In this study, the localization and appearance of synaptophysin-immunoreactive (IR) nerve cells and their relationships with the developing gastric layers were studied by immunocytochemistry and light microscopy in the embryonic rat stomach. The stomachs of Wistar rat embryos aged 13,21 days were used. The first neuronal bodies and their processes containing synaptophysin-immunoreactivity were observed on embryonic day 13. In contrast, synaptophysin-IR nerve terminals were first observed between mesenchymal cells on embryonic day 14. These results indicate that synaptophysin is expressed in growing neurits and neuronal cell bodies before these neurones have established synaptic connections. The occurrences of mesenchymal cell condensation near synaptophysin-IR neuroblasts on embryonic day 15 reflect an active nerve element-specific mesenchymal cell induction resulting in the morphogenesis of muscle cells. Similarly, the appearance of glandular structures after synaptophysin-IR neuroblasts, on embryonic day 18, suggests that the epithelial differentiation may be closely related to the neuronal maturation as well as other factors. Finally, synaptophysin is functionally important in neuronal development and maturation, together with the establishment of neuroneuronal and neuromuscular contacts and in epithelial differentiation. [source]


Potential antioxidant activity of celecoxib and amtolmetin guacyl: in vitro studies

AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2007
M. Kirkova
Summary 1,In vitro studies of the potential antioxidant activity of the selective cyclo-oxygenase-2 inhibitor celecoxib and the non-steroid anti-inflammatory drug amtolmetin guacyl (AMG) were carried out. The study included experiments on the ability of these drugs to affect some indices of the oxidative stress [lipid peroxidation (LP), activity of antioxidant enzymes, glutathione (GSH) level] in rat stomach and colon mucosa and in liver. 2,Celecoxib and AMG did not change the activity of the enzymes GSH-peroxidase, oxidased glutathione (GSSG)-reductase and glucose-6-phosphate-dehydrogenase, as well as the GSH level in all tissue preparations. An increased superoxide dismutase (SOD) activity and a tendency to a decreased Fe/ascorbic acid-induced LP in stomach and colon mucosa were found, but only in the presence of AMG. 3,In the liver, both celecoxib and AMG decreased spontaneous and Fe/ascorbic acid-induced LP. SOD activity was enhanced only in the presence of AMG. 4,Experiments aimed at studying celecoxib and AMG in free oxygen radical-generating systems were also carried out. AMG and tolmetin (the main metabolite of AMG) inhibited OH, -provoked deoxyribose degradation in a Fenton system. Celecoxib had no effect on free radicals when tested in the same system. 5,In conclusion, the results of the present in vitro studies suggest that AMG and celecoxib possess antioxidant and metal-chelating abilities, which might contribute to their beneficial effects. [source]


Appearance of Osteonectin-expressing Fibroblastic Cells in Early Rat Stomach Carcinogenesis and Stomach Tumors Induced with N-Methyl-N,-nitro-N-nitrosoguanidine

CANCER SCIENCE, Issue 9 2002
Hack-Young Maeng
The present study was designed to define molecular alterations in the initiation stage of rat stomach carcinogenesis. Groups of male Lewis rats, 6 weeks old, were given drinking water with or without N-methyl-N,-nitro-N-nitrosoguanidine (MNNG; 100 mg/liter). Total RNA was isolated from the stomach pyloric mucosa, and fluorescent differential display analysis was performed. A cDNA fragment of 125 bp encoding an extracellular matrix-associated matricellular glycoprotein, osteonectin, was identified after 14 days of MNNG exposure. A severalfold increase in expression was observed after 14 and 27 days of MNNG exposure, as determined by northern blot and RT-PCR. Immunohistochemistry revealed that osteonectin-mAb-stained flbroblastic cells appeared in interstitial tissue of pyloric mucosa. Additionally the gene expression of other extracellular matrix proteins, viz., collagen type III, fibronectin, osteopontin, proteoglycan NG2, laminin ,1 and S-laminin, was also markedly increased, as determined by competitive RT-PCR after 14 days of MNNG exposure. The gene expression of osteonectin and the six other extracellular matrix proteins was elevated in twelve stomach adenocarcinomas and adenomas induced by MNNG in Lewis and WKY rats. Osteonectin-mAb-stained flbroblastic cells were evident in interstitial tissue of stomach tumor. These results suggest that osteonectin-expressing flbroblastic cells appear in the interstitial tissue of pyloric mucosa from the early initiation stage of rat stomach chemical carcinogenesis, and that this phenomenon probably plays a role in cancer development. [source]


Interactive roles of endogenous prostaglandin and nitric oxide in regulation of acid secretion by damaged rat stomachs

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000
K. Takeuchi
Summary Background: The acid inhibitory mechanism in the damaged stomach is known to involve endogenous nitric oxide (NO) as well as prostaglandin (PG). Aim: To investigate the interaction between PG and NO in regulation of acid secretion in the stomach following damage. Methods: Under urethane anaesthesia, a rat stomach was mounted in an ex vivo chamber and perfused with saline. Acid secretion, luminal PGE2, NO metabolites (NOx) and histamine output were measured before and after application of 20 m m taurocholate Na (TC) for 30 min, with or without pre-treatment with indomethacin and/or NG -nitro- l -arginine methyl ester (L-NAME). Results: Exposure of the stomach to TC caused a decrease in acid secretion, with concomitant increase of both luminal NOx and PGE2. Either L-NAME or indomethacin reduced the decrease in acid secretion in response to TC, but only L-NAME allowed acid secretion to increase over basal values. L-NAME prevented the increase of luminal NOx after TC treatment, while indomethacin inhibited PGE2 release during and after exposure to TC. The increase in acid secretion in the presence of L-NAME was prevented when indomethacin was given concomitantly. TC treatment increased histamine output in the lumen, a process that was enhanced by L-NAME but reduced by indomethacin. Conclusions: Damage to the stomach increases both NO and PG in the lumen, and decreases acid secretion. Inhibiting NO production increases acid secretion in the damaged stomach, but only when PG biosynthesis is intact. It is assumed that endogenous PG has a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect probably through enhancing the release of mucosal histamine. [source]