Cells Of Rat Stomach Research Articles

Gastroprotective Effect of Combinations of Cincau Leaves and Mangosteen Peel on Ethanol-Induced Gastric Damage

Gastric ulcer is still a health problem in Indonesia. The leaves of cincau (Cyclea barbata Miers) and mangosteen peel (Garcinia mangostana Linn) have been investigated to have gastroprotective effects. This study aims to determine the effect of gastroprotector from the combination of Cincau leaves and mangosteen peel. This study used the post test only control group design. Wistar male rats were divided into 6 groups. Group I was a healthy control group and the second group was an untreated negative control. Group III is positive group treated with Ranitidine (0.016 g / kg BW). Groups IV, V, and VI were given green leaves of cincau (13.5 g / kg BW), mangosteen peel (25 g / kg BW) and 1: 1 combination. Treatment was performed for 14 days. On day 14 1 hour after treatment, all groups (except group I) were given 96% oral ethanol induction at a dose of 5 g / kg BW. On the 15th day the animals were sacrificed by means of anesthesia using chloroform. The area of the tukak is calculated by ImageJ and then calculates the index parameters of the ulcer and the protection ratio. The stomach is made of a hitopathologic preparation with Hematoxylin and Eosin (HE) and Immunohistochemistry (IHC) preparations to observe COX-2 expression. The index data of ulcer, protection ratio, gastric mucosal damage score and number of cells expressing COX-2 were statistically analyzed by SPSS program. The results showed that the combination of green leaves and mangosteen leaf ratio of 1: 1 had a gastroprotective effect by inhibiting the gastric induced index, increasing the ratio of protection, reducing total mucosal damage and inhibiting the expression of COX-2 protein in rat stomach cells significantly (p <0 , 05). Giving combination of Cincau leaf and mangosteen peal of 1: 1 able to give gastroprotective effect.

Distribution of ghrelin-positive mast cells in rat stomach

ABSTRACTIt is known that the gastrointestinal peptide hormone ghrelin is expressed in human and rodent B lymphocytes, T lymphocytes, monocytes and natural killer cells. However, there are no data about ghrelin expression by mast cells. These facts, as well as the common progenitor cells of mast cells and the above-mentioned immune cells, motivated us to undertake the current work in order to prove that like other granulocytes, rat gastric mast cells are capable of immunohistochemical expression of ghrelin. Gastric wall sections of Wistar rats were studied immunohistochemically for detection of ghrelin and tryptase and histochemically for toluidine blue in order to identify ghrelin-positive mast cells as well as to establish their localization and distribution. Results showed that mast cell granules expressed ghrelin. The ghrelin-positive mast cells were the least numerous as compared to tryptase-positive mast cells and toluidine blue-positive mast cells. Based on the observed expression of ghrelin in granules of mast cells localized in the rat gastric wall, we suggested that this type of cell can be regarded as an important source of ghrelin and suggested that ghrelin may exert different physiological functions, such as regulation of muscular, epithelial and glandular functions.

Effects of a hydrogen sulfide donor on spontaneous contractile activity of rat stomach and jejunum.

We studied the effect of sodium hydrosulfite (NaHS), a donor of hydrogen sulfide (H2S), on spontaneous contractive activity of isolated preparations of rat stomach and jejunum under isometric conditions. NaHS in concentrations of 10-200 μM reduced the amplitude, tonic tension, and frequency of contractions of the preparations. Blockade of K(+) channels with a non-specific antagonist tetraethylammonium (10 mM) increased contraction amplitude in the stomach strip and jejunum segment. The effects of NaHS on all parameters of contractile activity of the stomach and jejunum were fully preserved against the background of tetraethylammonium application. These data suggest that H2S in physiologically relevant concentrations inhibited spontaneous contractile activity of smooth muscle cells in rat stomach and jejunum by reducing the amplitude and frequency of contractions and decreased tonic tension without affecting the function of voltage- and calcium-dependent K(+) channels.

Localization of ANP-synthesizing cells in rat stomach

To study the morphological positive expression of antrial natriuretic peptide (ANP)-synthesizing cells and ultrastructural localization and the relationship between ANP-synthesizing cells and microvessel density in the stomach of rats and to analyze the distribution of the three histologically distinct regions of ANP-synthesizing cells. Using immunohistochemical techniques, we studied positive expression of ANP-synthesizing cells in rat stomach. A postembedding immunogold microscopy technique was used for ultrastructural localization of ANP-synthesizing cells. Microvessel density in the rat stomach was estimated using tannic acid-ferric chloride (TAFC) method staining. Distribution of ANP-synthesizing cells were studied in different regions of rat stomach histochemically. Positive expression of ANP-synthesizing cells were localized in the gastric mucosa of rats. Localization of ANP-synthesizing cells identified them to be enterochrochromaffin cells (EC) by using a postembedding immunogold electron microscopy technique. EC cells were in the basal third of the cardiac mucosa region. ANP-synthesizing cells existed in different regions of rat stomach and its density was largest in the gastric cardiac region, and the distribution order of ANP-synthesizing cells in density was cardiac region, pyloric region and fundic region in mucosa layer. We have also found a close relationship between ANP-synthesizing cells and microvessel density in gastric mucosa of rats using TAFC staining. ANP-synthesizing cells are expressed in the gastric mucosa. EC synthesize ANP. There is a close relationship between ANP-synthesizing cells and microvessel density in gastric mucosa of rats. The distribution density of ANP-synthesizing cells is largest in the gastric cardiac region.

Histamine and histidine decarboxylase are hallmark features of ECL cells but not G cells in rat stomach

The oxyntic mucosa of the rat stomach is rich in ECL cells which produce and secrete histamine in response to gastrin. Histamine and the histamine-forming enzyme histidine decarboxylase (HDC) have been claimed to occur also in the gastrin-secreting G cells in the antrum. In the present study, we used a panel of five HDC antisera and one histamine antiserum to investigate whether histamine and HDC are exclusive to the ECL cells. By immunocytochemistry, we could show that the ECL cells were stained with the histamine antiserum and all five HDC antisera. The G cells, however, were not stained with the histamine antiserum, but with three of the five HDC antisera. Thus, histamine and HDC coexist in the ECL cells (oxyntic mucosa) but not in G cells (antral mucosa). Western blot analysis revealed a typical pattern of HDC-immunoreactive bands (74, 63 and 54 kDa) in oxyntic mucosa extracts with all five antisera. In antral extracts, immunoreactive bands were detected with three of the five HDC antisera (same as above); the pattern of immunoreactivity differed from that in oxyntic mucosa. Food intake of fasted rats or treatment with the proton pump inhibitor omeprazole raised the HDC activity and the HDC protein content of the oxyntic mucosa but not of the antral mucosa; the HDC activity in the antrum was barely detectable. We suggest that the HDC-like immunoreactivity in the antrum represents a cross-reaction with non-HDC proteins and conclude that histamine and HDC are hallmark features of ECL cells but not of G cells.

Selenium-Dependent Glutathione Peroxidase-GI Is Localized in Basal Granulated Cells of Rat Stomach

Selenium-Dependent Glutathione Peroxidase-GI Is Localized in Basal Granulated Cells of Rat Stomach

Omeprazole-induced gene expression in oxyntic mucosa and ECL cells of rat stomach

Omeprazole-induced gene expression in oxyntic mucosa and ECL cells of rat stomach

Demonstration of muscarinic receptor mRNAs in parietal cells, enteric ganglia and immune cells of rat stomach by in situ hybridization histochemistry

Demonstration of muscarinic receptor mRNAs in parietal cells, enteric ganglia and immune cells of rat stomach by in situ hybridization histochemistry

Ultrastructure of enterochromaffin-like cells in rat stomach: effects of alpha-fluoromethylhistidine-evoked histamine depletion and hypergastrinemia.

Histamine-producing enterochromaffin-like (ECL) cells are numerous in the oxyntic mucosa of the rat stomach. They respond to gastrin by secretory activation, hypertrophy and hyperplasia. They contain cytoplasmic granules (median profile diameter 120 nm), secretory vesicles (180 nm) and microvesicles (70 nm). alpha-Fluoromethylhistidine (alpha-FMH) depletes histamine from the ECL cells by inhibiting the histamine-forming enzyme histidine decarboxylase. Long-term hypergastrinemia, evoked by omeprazole, increases the ECL-cell histamine concentration. The way in which chronic histamine depletion affects omeprazole-induced ECL-cell hypertrophy, and the ways in which granules and vesicles in the ECL cells respond to alpha-FMH and/or omeprazole have been studied. Rats were treated with alpha-FMH (3 mg/kg per h subcutaneously), omeprazole (400 micromol/kg per day orally), alpha-FMH+omeprazole, or vehicle for 6 weeks. ECL cell profiles in electron micrographs were analysed panimetrically. The results show that the omeprazole-evoked hypertrophy of the ECL cells is not affected by depletion of ECL-cell histamine, thereby supporting the view that ECL-cell histamine is not important for full expression of the gastrin-evoked trophic effects on the ECL cells. The loss of ECL-cell histamine following treatment with alpha-FMH and with alpha-FMH+omeprazole is associated with a greatly reduced size of the secretory vesicle compartment. The granules, on the other hand, are unaffected by alpha-FMH and alpha-FMH+omeprazole. Omeprazole treatment leads to the appearance of numerous vacuoles (with profile diameter greater than 500 nm); such vacuoles are not observed in the ECL cells of rats treated with alpha-FMH or alpha-FMH+omeprazole. The omeprazole-induced increase in ECL-cell histamine is associated with an increase in the compartment composed of secretory vesicles and vacuoles. The findings support the hypothesis that secretory vesicles (and vacuoles) represent a major storage site of ECL-cell histamine.

Evidence for nitric oxide production by enterochromaffinlike cells in rat stomach under hypergastrinemia induced by proton pump inhibitors

Evidence for nitric oxide production by enterochromaffinlike cells in rat stomach under hypergastrinemia induced by proton pump inhibitors

Purification and immunohistochemistry of Griffonia simplicifolia agglutinin-II-binding mucus glycoprotein in rat stomach.

Gastric mucus is thought to protect the gastric wall from mechanical trauma, desiccation, pathogenic microorganisms, acid and proteases. We purified Griffonia simplicifolia agglutinin-II (GSA-II)-binding mucus glycoprotein (GMG) from rat gastric mucosa by solubilization in a guanidine-containing buffer, gel permeation chromatography, Ricinus communis agglutinin-I (RCA-I)-affinity chromatography and GSA-II-affinity chromatography. Rat GMG showed high molecular weight on a Sephacryl S-1000 column, and a single band in 0.5% agarose-2% polyacrylamide composite gels and blots. A protein of approximately 60 kDa was contained in the GMG preparation. GMG was deglycosylated with trifluoromethanesulphonic acid treatment. An antibody was raised against deglycosylated GMG (deGMG). The antibody recognized deGMG, GMG, periodic acid-treated deGMG and O-glycanase-digested deGMG, but did not react to trypsin-digested deGMG. These results suggest that the antibody recognizes proteinase-sensitive region or peptide backbone of GMG. In immunohistochemistry, the mucous gel layer of the stomach luminal surface was stained with antibody. The antibody recognized not only gastric mucous neck cells and pyloric gland cells, but also gastric surface mucous cells, mucous cells in the duodenal gland, and goblet cells in the small intestine and colon. These results indicate that GMG is a component of rat gastric mucus, and that the antibody recognizes mucous-secreting cells in rat stomach and intestine.

Time-dependent changes in enterochromaffinlike cell kinetics in stomach of hypergastrinemic rats

Background: Hypergastrinemia has been claimed to cause first hyperplasia and then dysplasia/neoplasia of enterochromaffinlike (ECL) cells in rat stomach. The growth is thought to reflect an accelerated self replication rate of mature ECL cells. The cytokinetics and the histidine decarboxylase (HDC) activity of the ECL cells were investigated during sustained hypergastrinemia. Methods: Hypergastrinemia was evoked by omeprazole (400 μmol · kg−1 · day−1 orally) for up to 1 year. Immunocytochemistry for histamine was used to determine the ECL cell density and combined with [H3]thymidine autoradiography to establish the labeling index (LI), i.e., the proportion of the ECL cells that has incorporated [H3]thymidine. Results: The ECL cell density increased progressively for 10–20 weeks in response to the hypergastrinemia and remained at a plateau for the remainder of the study. The hyperplasia was diffuse with additional micronodules at 52 weeks. The ECL cell LI was maximally elevated after 1–2 weeks and declined to control values after 10–20 weeks of treatment. In contrast, the HDC activity remained elevated for the duration of the study. Conclusions: The ECL cell hyperplasia reflects the transiently elevated ECL cell LI during the early phase but is not associated with an accelerated rate of mitosis during the 10–52 weeks period. Even though with time gastrin seems to loose its ability to sustain a high ECL cell LI it retains its ability to maintain a high HDC activity.

Enterochromaffin-like Cells in Rat Stomach Respond to Short-Term Infusion of High Doses of Cholecystokinin But Not to Long-Term, Sustained, Moderate HyperCCKemia Caused by Continuous Cholecystokinin Infusion or Pancreaticobiliary Diversion

The histamine-producing enterochromaffin-like (ECL) cells in the oxyntic mucosa are controlled by gastrin. An acute gastrin challenge induces release and accelerated resynthesis of ECL cell histamine. Long-term stimulation with gastrin causes ECL cell hyperplasia. We set out to study whether the ECL cells respond not only to gastrin but also to cholecystokinin (CCK). A wide dose range of gastrin-14 sulfated and -17 non-sulfated and CCK-8 sulfated (CCK-8s) and non-sulfated (CCK-8) was infused intravenously to rats for 3 h. The activity of the histamine-forming enzyme was measured at termination of infusion. Gastrins and CCK-8s were equally effective in activating the enzyme, whereas sulfated CCK-8 was notably less potent than the other three peptides. Clearly, the receptor responsible for activation of the ECL cells distinguishes poorly between gastrin-17 and CCK-8s, which is in line with the characteristics of the CCK-B receptor. Moreover, neither the response to gastrin-17 nor that to CCK-8s was affected by concomitant infusion of devazepide (200 micrograms/kg/h), a selective CCK-A-receptor antagonist. One group of rats received CCK-8s continuously via a minipump. Another group of rats was subjected to pancreaticobiliary diversion (PBD), which increases the plasma CCK concentration 10- to 20-fold. The rats were killed 7 or 10 weeks later, respectively, and the stomachs were analyzed with regard to mucosal growth and ECL cell hyperplasia. HyperCCKemic rats had increased pancreatic weights but showed no signs of growth stimulation in the stomach and no ECL cell hyperplasia.(ABSTRACT TRUNCATED AT 250 WORDS)

Hyperplasia of histamine-depleted enterochromaffinlike cells in rat stomach using omeprazole and α-fluoromethylhistidine

In the rat, gastric histamine is stored mainly in the enterochromaffinlike cells. Gastrin releases histamine from these cells, and long-term hypergastrinemia results in hyperplasia. The effect of sustained hypergastrinemia on histamine-depleted enterochromaffinlike cells was studied by measuring histidine decarboxylase activity and histamine concentrations and by using quantitative histology. Hypergastrinemia maintained for 6 weeks was induced by inhibition of gastric acid secretion with omeprazole (400 μmol · kg−1 · day−1) given orally, and histamine synthesis was inhibited for the same length of time with α-fluoromethylhistidine (3 mg · kg−1 · h−1) given via osmotic minipumps. In rats given omeprazole alone, the effects of the resulting hypergastrinemia on the enterochromaffinlike cells was reflected in increased histidine decarboxylase activity, increased histamine concentration, and increased number of enterochromaffinlike cells. The general trophic effects on the stomach were seen as increased stomach and oxyntic mucosal weight and increased mucosal thickness. Treatment with a-fluoromethylhistidine plus omeprazole markedly reduced the histidine decarboxylase activity and histamine concentration, but the weight of the stomach and oxyntic mucosa, the enterochromaffinlike cell density, and intensity of histidine decarboxylase immunostaining were increased to at least the same extent as after omeprazole alone. These observations indicate that enterochromaffinlike cell histamine is not important for a full expression of gastrin-evoked trophic effects in the stomach.

Ontogeny of histamine-immunoreactive cells in rat stomach.

An antiserum against hemocyanin-conjugated histamine was used to study the cellular stores of histamine in the stomach, especially the oxyntic mucosa, of fetal and early postnatal rats. Tissues were fixed in 4% 1-ethyl-3(3-dimethyl-aminopropyl) carbodiimide (EDC-DI) and standard immunofluorescence technique was used. Histamine was first detected on the 16th embryonic (E16) day when a few histamine-immunoreactive (HA-ir) cells and nerve fibers were observed in the muscular layer of the stomach wall. On day E18, HA-ir cells were visualized for the first time in the oxyntic mucosa of the stomach, and from that day on the number of such cells increased slowly initially and after day E20 more rapidly. At birth many of the HA-ir cells in the oxyntic mucosa possessed processes giving them a paracrine-like appearance typical of enterochromaffin-like cells (ECL cells). Only a very small number of the HA-ir cells represented metachromatically stained mast cells and were located in the submucosa. After birth, the number of HA-ir ECL cells increased steadily, until day 21 when the distribution and number was very similar to that of the adult. The results suggest that histamine-containing neurons and ECL cells appear in the stomach wall before birth, and that there are histamine-containing ECL cells in the mucosa and mast cells in the submucosa of the stomach wall at birth.

Omeprazole and ranitidine, antisecretagogues with different modes of action, are equally effective in causing hyperplasia of enterochromaffin-like cells in rat stomach

Female rats were treated for 28 days with high doses of the gastric acid secretion inhibitors omeprazole and ranitidine. Omeprazole, which is long-acting, was given orally once daily. Ranitidine, which is short-acting, was given by continuous infusion (via osmotic minipumps, implanted subcutaneously). The aim was to produce a similar degree of acid inhibition with the two drugs. The inhibition of acid secretion over the day and night was more pronounced in the omeprazole-treated rats (maximal inhibition 100%, minimum 85%) than in those receiving ranitidine (mean 70%). In both groups, there was a great increase in plasma gastrin, somewhat greater after omeprazole than after ranitidine. The gastrin concentration in the antrum was almost doubled by both treatments and there was a moderate increase in the number of antral gastrin cells in the omeprazole-treated rats. The number of enterochromaffin-like (ECL) cells (per visual field) increased in the oxyntic mucosa to the same extent (> 100%) in the ranitidine- and omeprazole-treated rats. Apart from the gastrin cells in the antrum and the ECL cells in the corpus no other gastric endocrine cell type seemed to respond to treatments with antisecretagogues. We conclude that, regardless of the type of antisecretagogue used, effective and long-term suppression of gastric acid secretion results in sustained hypergastrinemia and increased number of ECL cells. Conceivably therefore, the ECL cell hyperplasia reflects the trophic effect of gastrin.

Proliferative activity of gastric and duodenal endocrine cells in the rat

The replicative activity and migration of gastrin, somatostatin and serotonin cells in rat stomach and duodenum was studied using combined immunocytochemistry and autoradiography after 3H thymidine pulse-labeling. Our results show that a small proportion of gastrin, somatostatin and serotonin immunoreactive cells displays proliferative activity. The overall labeling index ranged from 1.3% for gastric endocrine cells to 3.2% for duodenal endocrine cells. In a pulse chase experiment, labeling indices of immunoreactive cells were estimated at several time intervals after 3H thymidine administration. Significant differences in labeling index were not found. Migration of 3H thymidine labeled endocrine cells towards the luminal surface was not found in the stomach nor in the duodenum. It is concluded that 1) these endocrine cells have replicating activity; 2) the replicative activity of endocrine cells is higher in the duodenum than in the stomach; 3) the various cell types do not show significant differences in replicating activity and 4) endocrine cells did not seem to migrate to the luminal surface of the mucosa along with the other epithelial cells.

Cells intermediate between mucous neck cells and chief cells in rat stomach.

Morphological and histochemical methods revealed cells intermediate between mucous neck cells and chief cells in rat stomach. The secretory granules of mucous neck cells and chief cells were homogeneous. However, some cells resembling mucous neck cells in shape and size yet contained heterogeneous granules. One type of cell contained mucous granules showing a bipartite structure. The inner cores of these granules resembled the granules of mucous neck cells morphologically and after staining by the periodic acid-thiocarbohydrazide-silver proteinate (PA-TCH-SP) procedure and lectin-ferritin methods. The outer layer of these granules, however, resembled the granules of chief cells and failed to stain by these methods. Another type of cell also contained bipartite granules, but these showed a dense cap and lucent matrix. The cap of the granules did not stain with the PA-TCH-SP and lectin methods, but the remaining matrix was reactive. These presumed transitional cells were located in a layer between the mucous neck cells and the chief cells. Immature chief cells with sparse granular reticulum were found near these intermediate cells in some cases. Many similar intermediate type cells were also found in early developmental stages of the gastric mucosa in rat. These results suggest a close relationship between chief cells and mucous neck cells; chief cells may develop from undifferentiated stem cells via mucous neck cells in adult rat stomach.

Effects of bilateral nephrectomy on endocrine cells of rat stomach [proceedings

These changes seem to accord with activation of the ECL and A-like cells and deactivation of the parietal cells. The results suggest that the G cells are probably also deactivated, conceivably by auto-feedback resulting from the hypergastrinaemia.

Effects of Bilateral Nephrectomy on Endocrine Cells of Rat Stomach

It has previously been shown that in the rat nephrectomy is followed by hypergastrinemia, elevated histidine decarboxylase activity, and lowered histamine content in the gastric mucosa; paradoxically this is accompanied by low gastric acid secretion and lack of response to pentagastrin. The present report deals with the morphological changes in the histamine-containing cells, gastrin (G) cells, and the parietal cells after nephrectomy. The number of gastric enterochromaffin, enterochromaffin-like and G cells was assessed by fluorescence histochemistry. In addition, the concentration of 5-HT in the pyloric mucosa and of histamine in the oxyntic mucosa was determined. Under the fluorescence microscope the enterochromaffin-like cells appeared reduced in number (p < 0.001) corresponding with significant lowering of gastric mucosal histamine content (p < 0.01) after nephrectomy. The number of enterochromaffin cells and gastrin cells was not affected, neither was the 5-HT content. The histamine-containing enter...