Gastric Glandular Mucosa Research Articles

Equine gamma herpesvirus presence and viral load are not associated with equine glandular gastric disease.

To investigate the role of equine herpesvirus-2 (EHV-2) and equine herpesvirus-5 (EHV-5) in equine glandular gastric disease (EGGD) by visualizing and quantifying these gamma herpesviruses in EGGD-affected and normal glandular gastric mucosa of horses. A secondary objective was to describe the histopathological abnormalities in the equine gastric glandular mucosa in horses with EGGD. 29 horses (n = 21 postmortem and 8 gastroscopy) categorized as normal (11), EGGD (12), or both EGGD and equine squamous gastric disease (6). Glandular gastric mucosal samples were collected from horses by gastroscopy or postmortem. Histopathology and in situ hybridization targeting EHV-2 and EHV-5 were performed on grossly normal and abnormal glandular gastric mucosa. The number of in situ hybridization-positive cells per millimeter squared of tissue was calculated. Evaluators were blinded to groups. Glandular gastric tissues from horses without EGGD had higher viral loads in the mucosa than normal or abnormal tissues from EGGD horses. There was no difference in viral loads for EHV-2 or EHV-5 between grossly or endoscopically normal to abnormal gastric tissues within horses with EGGD. Lymphocytic plasmacytic gastritis was the most common histopathological abnormality, with only 3 horses having mucosal disruption (glandular ulcer or erosion). Equine gamma herpesviruses are unlikely to play a role in the pathophysiology of EGGD. EGGD is frequently inflammatory with occasional mucosal disruption (ulcer or erosion).

Field study examining the mucosal microbiome in equine glandular gastric disease

Equine glandular gastric disease (EGGD) is a common disease among athletic horses that can negatively impact health and performance. The pathophysiology of this EGGD remains poorly understood. Previous studies using controlled populations of horses identified differences in the gastric glandular mucosal microbiome associated with disease. The objective of this study was to compare the gastric microbiome in horses with EGGD and those without across multiple barns and differing management practices. We hypothesized that alterations in the microbiome of the gastric glandular mucosa are associated with EGGD. A secondary objective was to perform a risk factor analysis for EGGD using the diet and management data collected. Microbial populations of biopsies from normal pyloric mucosa of horses without EGGD (control biopsies), normal pyloric mucosa of horses with EGGD (normal biopsies) and areas of glandular mucosal disruption in horses with EGGD (lesion biopsies) were compared. Lesion biopsies had a different microbial community structure than control biopsies. Control biopsies had a higher read count for the phylumActinomycetotacompared to lesion biopsies. Control biopsies also had an enrichment of the generaStaphylococcusandLawsonellaand the speciesStreptococcus salivarius. Lesion biopsies had an enrichment of the generaLactobacillusandActinobacillusand the speciesLactobacillus equigenerosi. These results demonstrate differences in the gastric glandular microbiome between sites of disrupted mucosa in horses with EGGD compared to pyloric mucosa of horses without EGGD. Risk factor analysis indicated that exercise duration per week was a risk factor for EGGD.

Gastric ulcer in horses

Equine gastric ulcer comprises a complex of diseases associated with ulceration of the esophageal, gastric or duodenal mucosa. Ulceration occurs on nonglandular (squamous) and glandular gastric mucosa, with an average prevalence of 5% in pasture horses, 93% in racehorses and between 25% and 57% in foals. The incriminated causes are diet and incorrect feeding, stress and the administration of anti-inflammatory drugs (NSAIDs). Medication for gastric ulcers includes proton pump inhibitors, histamine (H2) receptor antagonists, prostaglandin analogs, and sucralfate.

S3716 A Rare Case of Ectopic Liver Tissue Incidentally Found in the Gastric Body

Introduction: Ectopic liver tissue (ELT) is seldom reported in the literature. It is usually asymptomatic and incidentally found. However, ELT has a strong association with malignant transformation to hepatocellular carcinoma (HCC), making removal of this tissue essential. Presented is a rare case of ELT found in the stomach. Case Description/Methods: A 78-year-old male with a past medical history of hypertension and gastritis presented to clinic for worsening gastroesophageal reflux disease (GERD) over the past six months. The patient reported GERD symptoms for the past twenty years that he had been self-treating with over-the-counter proton pump inhibitors, probiotics, and digestive enzymes without relief. On presentation his vitals, physical exam, and blood work were unremarkable. The patient underwent esophagoduodenoscopy (EGD) which revealed esophagitis, a large paraesophageal hernia, and a single 15-millimeter submucosal nodule in the anterior wall of the gastric body. Cold forceps biopsies obtained from the body and antrum of the stomach were unremarkable and negative for H. pylori. He was referred for endoscopic ultrasound (EUS), where a fine needle biopsy of the benign-appearing gastric body submucosal nodule was performed (figure 1a). Three passes were made with a 22-gauge ultrasound biopsy needle using a transgastric approach. A visible core of tissue was obtained. Final cytology demonstrated superficial gastric mucosa and detached benign liver tissue (figures 1b, 1c). No dysplasia or malignancy was seen. Discussion: ELT has an incidence of 0.24-0.47%. Of the reported cases, ELT is most commonly seen in the gallbladder or pancreas. The etiology of ELT is unknown but is thought to be associated with errors in embryological development. Most ELT is asymptomatic but can develop the same pathologies as the orthotopic liver. It can also cause abdominal pain, bleeding, and compression of neighboring tissues. There is also a strong association between HCC and ELT, necessitating biopsy and endoscopic removal. This case demonstrated ELT incidentally found in the gastric body during EGD and was biopsied by a fine needle using EUS guidance. Histology was without features to suggest malignancy, but to prevent malignant transformation endoscopic resection was recommended.Figure 1.: 1a. Arrow indicating nodule in gastric body, as seen by endoscopic ultrasound. Image 1b. Hematoxylin and eosin stain with 100x magnification. Normal gastric glandular mucosa. Arrow indicating benign unremarkable hepatic tissue found in gastric body. Image 1c. Hematoxylin and eosin stain with 200x magnification. Benign unremarkable hepatic tissue found in gastric body.

Presence of Helicobacter spp. in dental tartar and gastric mucosa, and its relationship with EGUS in horses from a public slaughterhouse

Background: Despite the fact that Helicobacter spp. has been detected in equine gastric mucosa, no evidence exists about this infection in Colombian horses affected by equine ulcerative gastric syndrome (EGUS), nor in dental tartar. Objective: To detect Helicobacter spp. DNA in equine gastric mucosa and dental tartar and determine the relationship between the presence of Helicobacter spp. and gastric lesions. Methods: Samples of glandular gastric mucosa and dental tartar were collected from 30 equine slaughterhouses. Macroscopic lesions of the stomachs were classified and the total DNA in all samples was extracted using a commercial extraction kit. A final-point PCR was performed using primers for amplification of a segment of 251 bp of the gene encoding the 16s rRNA region; the amplified fragments were subjected to a second PCR to determine the presence of H. pylori, the VacA gene was typified. The resulting amplicons were sequenced. Results: It was possible to amplify 16s rRNA in several samples but there was no amplification of VacA. Fragments of the sequences were compatible with H. heilmannii. The 23.3 and 10% of gastric and tartar samples were positive for 16s rRNA of Helicobacter spp., respectively. Conclusion: Although genetic material of Helicobacter spp. was found in some animals, there was no relationship with gastric lesions. It is possible that helicobacteriosis has no bearing in EGUS etiology.

Effect of oral administration of omeprazole on the microbiota of the gastric glandular mucosa and feces of healthy horses.

BackgroundOmeprazole administration is associated with changes in gastric and fecal microbiota and increased incidence of Clostridioides difficile enterocolitis in humans and dogs.Hypothesis/ObjectivesStudy purpose was to assess the effect of omeprazole on gastric glandular and fecal microbiota in healthy adult horses.AnimalsEight healthy horses stabled on straw and fed 100% haylage.MethodsProspective controlled study. Transendoscopic gastric glandular biopsies, gastric fluid, and fecal samples were obtained from each horse twice at a 7‐day interval before the administration of omeprazole. Samples were taken on the same horses before and after a 7‐day administration of omeprazole (4 mg/kg PO q24h). pH was assessed on fresh gastric fluid and other samples were kept at −20°C until analysis. Bacterial taxonomy profiling was obtained by V1V3 16S amplicon sequencing from feces and gastric glandular biopsies. Analysis of alpha, beta diversity, and comparison between time points were performed with MOTHUR and results were considered significant when P < .05.ResultsGastric pH increased significantly after 7 days of omeprazole administration (P = .006). Omeprazole did not induce significant major changes in composition of fecal or gastric glandular microbiota, however, after administration, certain microbial genera became more predominant in the gastric glandular mucosa (lower Simpson's evenness, P = .05). Only the genus Clostridium sensu strictu_1 had a significant shift in the glandular gastric mucosa after omeprazole administration (P = .002). No population shifts were observed in feces.Conclusions and Clinical ImportanceOral administration of omeprazole could have fewer effects in gastrointestinal microbiota in the horse compared to other species.

Comparison of the gastric fluid and glandular mucosa and microbiome in horses with and without equine glandular gastric disease (EGGD)

Comparison of the gastric fluid and glandular mucosa and microbiome in horses with and without equine glandular gastric disease (EGGD)

Does prebiotic feeding affect equine gastric health? A study on the effects of prebiotic-induced gastric butyric acid production on mucosal integrity of the equine stomach

Fructo-oligosaccharides are commonly administered as prebiotics to horses in order to reduce the risk of disruption of microbial populations in the hindgut. Their microbial degradation to SCFA already begins in the stomach potentially resulting in increased gastric concentrations of SCFA such as butyric acid. The impact of butyric acid on the squamous mucosa is postulated to be detrimental, its effects on the glandular mucosa are yet unknown. Thus, the aim of this study was to determine the effects of butyric acid exposure on the functional integrity and morphology of the equine nonglandular and glandular gastric mucosa using butyric acid concentrations equivalent to the ones found in horses subjected to prebiotic fructo-oligosaccharides feeding. Gastric mucosal samples of healthy horses were exposed to butyric acid using the in vitro Ussing chamber technique. Electrophysiological parameters were continuously monitored, mucosal samples were blinded and histomorphological analysis was performed using a scoring system for assessment of histopathologic changes. Exposure to butyric acid resulted in pathohistomorphological changes in the glandular mucosa and in impairment of functional mucosal integrity in the squamous and the glandular mucosa as documented by significant changes in tissue conductances (Gt). Administration of fructo-oligosaccharides as a preventive prebiotic measure to horses should therefore be carefully considered, particularly in horses known to be at risk of developing EGUS.

Gastroprotective activity of a novel Schiff base derived dibromo substituted compound against ethanol-induced acute gastric lesions in rats

BackgroundBasic function of bromine in body is to activate pepsin production in gastritis with low acidity. The present study encompasses a broad in vivo study to evaluate gastroprotective activity of a novel dibromo substituted Schiff base complex against Sprague Dawley (SD) rats.Methods2, 2′-[1, 2-cyclohexanediylbis (nitriloethylidyne)]bis(4-bromophenol) (CNBP) is synthesized via a Schiff base reaction, using the related ketone and diamine as the starting materials. SD rats are divided as normal, ulcer control (5 ml/kg of 10% Tween 20), testing (10 and 20 mg/kg of CNBP) and reference groups (omeprazole 20 mg/kg). Except for the normal group, the rest of the groups are induced gastric ulcer by ethanol 1 h after the pre-treatment. Ulcer area, gastric wall mucus, and acidity of gastric content of the animal stomachs are measured after euthanization. Antioxidant activity of the compound is tested by Ferric reducing antioxidant power (FRAP) test and safety of the compound is identified through acute toxicity by [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Moreover, activities of superoxide dismutase (SOD), catalase (CAT), levels of prostaglandins E2 (PGE2) and also malondialdehyde (MDA) are determined.ResultsAntioxidant activity of CNBP was approved via FRAP assay. Vast shallow hemorrhagic injury of gastric glandular mucosa was observed in the ulcer group compared to the CNBP-treated animals. Histological evaluations confirmed stomach epithelial defense effect of CNBP with drastic decrease of gastric ulceration, edema and leucocytes penetration of submucosal stratum. Immunostaining exhibited over-expression in HSP70 protein in CNBP-treated groups compared to that of the ulcer group. Also, gastric protein analysis showed low levels of MDA, PGE2 and high activity of SOD and CAT.ConclusionsCNBP with noticeable antioxidant property showed gastroprotective activity in the testing rodents via alteration of HSP70 protein expression. Also, antioxidant enzyme activities which were changed after treatment with CNBP in the animals could be elucidated as its gastroprotective properties.

Biochanin a gastroprotective effects in ethanol-induced gastric mucosal ulceration in rats.

BackgroundBiochanin A notable bioactive compound which is found in so many traditional medicinal plant. In vivo study was conducted to assess the protective effect of biochanin A on the gastric wall of Spraguedawley rats` stomachs.MethodologyThe experimental set included different animal groups. Specifically, four groups with gastric mucosal lesions were receiving either a) Ulcer control group treated with absolute ethanol (5 ml/kg), b) 20 mg/kg of omeprazole as reference group, c) 25 of biochanin A, d) 50 mg/kg of biochanin A. Histopathological sectioning followed by immunohistochemistry staining were undertaken to evaluate the influence of the different treatments on gastric wall mucosal layer. The gastric secretions were collected in the form of homogenate and exposed to superoxide dismutase (SOD) and nitric oxide enzyme (NO) and the level of malondialdehyde (MDA) and protein content were measured. Ulceration and patchy haemorrhage were clearly observed by light microscopy. The morphology of the gastric wall as confirmed by immunohistochemistry and fluorescent microscopic observations, exhibited sever deformity with notable thickness, oedematous and complete loss of the mucosal coverage however the biochanin-pretreated animals, similar to the omeprazole-pretreated animals, showed less damage compared to the ulcer control group. Moreover, up-regulation of Hsp70 protein and down-regulation of Bax protein were detected in the biochanin A pre-treated groups and the gastric glandular mucosa was positively stained with Periodic Acid Schiff (PAS) staining and the Leucocytes infiltration was commonly seen. Biochanin A displayed a great increase in SOD and NO levels and decreased the release of MDA.ConclusionsThis gastroprotective effect of biochanin A could be attributed to the enhancement of cellular metabolic cycles perceived as an increase in the SOD, NO activity, and decrease in the level of MDA, and also decrease in level of Bax expression and increase the Hsp70 expression level.

Rethinking equine gastric ulcer syndrome: Part 3 – Equine glandular gastric ulcer syndrome (EGGUS)

SummaryIt has recently been highlighted that significant differences exist between ulceration of the squamous gastric mucosa and ulceration of the glandular gastric mucosa in the horse. The first article in this series discussed terminology, clinical signs and diagnosis and the second reviewed ulceration of the squamous gastric mucosa in detail. The purpose of this article, the third and last in the series, is to review the pathophysiology, risk factors, prevalence, treatment and prevention of ulceration of the glandular gastric mucosa.

Rethinking equine gastric ulcer syndrome: Part 2 – Equine squamous gastric ulcer syndrome (ESGUS)

SummaryIt has recently been highlighted that significant differences in prevalence, risk factors and the response to treatment exist between ulceration of the squamous gastric mucosa and ulceration of the glandular gastric mucosa in the horse. In the first article in the series, the term equine squamous gastric ulcer syndrome (ESGUS) was used to describe disease of the squamous gastric mucosa with clinical signs and diagnosis discussed. The purpose of this article is to review the pathophysiology, risk factors, prevalence, treatment and prevention of ESGUS.

Orally administered phenylbutazone causes oxidative stress in the equine gastric mucosa.

Phenylbutazone (PBZ) is widely used in equine medicine, and its side effects on the gastrointestinal tract are well known. The inhibition of prostaglandins and the oxidative stress induced by nonsteroidal anti-inflammatory drugs (NSAIDs) are described as mechanisms of gastric mucosal injury in humans. In horses, only the secondary effect of changes in cyclooxygenases is related to gastric mucosal injury. The objective of this study was to evaluate the effect of PBZ on certain antioxidative/oxidative parameters of the gastric mucosa. The concentrations of antioxidants and oxidants (superoxide dismutase, SOD; catalase, CAT; nitric oxide, NO; total glutathione, GSH; myeloperoxidase, MPO; and malondialdehyde, MDA), PGE2 levels, and the ulcerative lesions score were assessed. The results demonstrated decreased levels of antioxidant variables, increased levels of oxidant variables, and alterations in the prostaglandin E2 (PGE2 ), myeloperoxidase (MPO), and glutathione (GSH) levels. In conclusion, PBZ induces oxidative stress in the gastric glandular mucosa of horses by changing the antioxidant-oxidant balance of this surface, which might be regarded as another mechanism of injury in the horse stomach.

Specific enrichment of the RNA-binding proteins PCBP1 and PCBP2 in chief cells of the murine gastric mucosa

RNA-binding proteins and corresponding post-transcriptional controls play critical roles in gene expression. The poly-(C) binding proteins, PCBPs (αCPs, hnRNPEs), comprise a well-characterized family of abundant RNA-binding proteins that impact on RNA processing in the nucleus as well as mRNA stability and translation in the cytoplasm. Here we demonstrate that PCBP1 and PCBP2 are abundantly expressed in the gastric epithelium with prominent enrichment in specific cell types within the gastric glandular mucosa. The spatial and intracellular patterns of PCBP1 and PCBP2 expression in these regions are highly correlated. Remarkably, we observe that these proteins are present in the nuclear and cytoplasmic compartments of zymogenic chief cells while they are restricted to the nuclear compartment in acid-secreting parietal cells and poorly expressed in pit cells that line the gland exit. This specificity of expression patterns and subcellular localization of PCBP1 and PCBP2, along with their appearance in the precursor tissues of the gastric epithelium during early postnatal development, suggests these RNA-binding proteins play specific roles in cell differentiation and organismal development within the gastric glandular epithelium.

Effects of phenylbutazone on gene expression of cyclooxygenase-1 and -2 in the oral, glandular gastric, and bladder mucosae of healthy horses

To assess gene expressions of cyclooxygenase-1 and -2 in oral, glandular gastric, and urinary bladder mucosae and determine the effect of oral administration of phenylbutazone on those gene expressions in horses. 12 healthy horses. Horses were allocated to receive phenylbutazone or placebo (6 horses/group); 1 placebo-treated horse with a cystic calculus was subsequently removed from the study, and those data were not analyzed. In each horse, the stomach and urinary bladder were evaluated for ulceration via endoscopy before and after experimental treatment. Oral, glandular gastric, and urinary bladder mucosa biopsy specimens were collected by use of a skin punch biopsy instrument (oral) or transendoscopically (stomach and bladder) before and after administration of phenylbutazone (4.4 mg/kg, p.o., q 12 h) in corn syrup or placebo (corn syrup alone) for 7 days. Cyclooxygenase-1 and -2 gene expressions were determined (via quantitative PCR techniques) in specimens collected before and after the 7-day treatment period and compared within and between groups. Prior to commencement of treatment, biopsy specimens from 7 horses were used to compare gene expressions among tissues. The cyclooxygenase-1 gene was expressed in all tissues collected. The cyclooxygenase-2 gene was expressed in the glandular gastric and bladder mucosae but not in the oral mucosa. Cyclooxygenase gene expressions were unaffected by phenylbutazone administration. Cyclooxygenase-2 was constitutively expressed in glandular gastric and bladder mucosae but not in the oral mucosa of healthy horses. Oral administration of phenylbutazone at the maximum recommended dosage daily for 7 days did not affect cyclooxygenase-1 or -2 gene expression.

The influence of chronic or acute nicotine pretreatment on ethanol-induced gastric ulceration in the rat

The effects in rats of chronic or acute nicotine pretreatment were studied on three gastric parameters: ethanol-induced ulceration, gastric wall mucus content and gastric acid secretion, under basal or histamine-stimulated conditions. Oral administration of ethanol (40%, 10 ml kg-1) depleted gastric wall mucus and produced ulceration in the gastric glandular mucosa. Ten-day nicotine pretreatment (15 or 25 micrograms ml-1 drinking water) worsened the adverse effects of ethanol on mucosal ulceration and mucus content, potentiated the gastric secretory action of histamine, but did not affect basal acid secretion. Single oral doses of nicotine (2 or 4 mg kg-1, given 1 h beforehand) prevented ulceration and mucus depletion in ethanol-treated animals; however, they did not influence either basal or histamine-stimulated gastric acid output. It is concluded that chronic nicotine administration aggravates ethanol ulceration, possibly by decreasing gastric wall mucus content and sensitizing the stomach to the acid secretory action of histamine. On the other hand, an acute oral dose of nicotine preserves the mucus content and prevents ethanol-induced ulcer formation.

Permeation studies on freshly excised rat gastric mucosa: influence of pH

The objective of this study was to evaluate the influence of pH on the permeation of model drugs through freshly excised rat stomach. Additionally, the capability of excised gastric mucosa to maintain an acidic pH was assessed. In vitro permeation studies were performed in Ussing-type diffusion chambers with rat stomach using fluorescence-labeled bacitracin (bac-FITC), sodium fluorescein (NaFlu), propranolol HCl, and cimetidine as model drugs. The pH was adjusted to pH 1, 2, and 6.8 in the donor chamber and pH 7.4 in the acceptor chamber. The study demonstrated that both, the fore stomach and the glandular gastric mucosa, are capable of maintaining an acidic pH of 1–1.2 in the donor chamber. Papp (permeation coefficients) were found to be 1.4 ± 0.6 ×·10−7 and 7.6 ± 0.7 ×·10−7 for bac-FITC and 3.3 ± 1.5 ×·10−7 and 2.4 ± 0.6 ×·10−6 cm/sec for NaFlu at pH 2 and 6.8, respectively, in the glandular stomach. In order to evaluate the effect of pH on the integrity of paracellular space, propranolol as high-permeability drug and cimetidine as low-permeability drug were chosen. The Papp of propranolol HCl was determined to be 5.9 ± 0.3 ×·10−7 and 1.1 ± 0.7 ×·10−6 cm/sec at pH 2 and 6.8, respectively, in the glandular stomach. Cimetidine showed a permeability of 1.4 ± 0.4 ×·10−5 and 9.6 ± 2.3 ×·10−6 cm/sec at pH 2 and 6.8. Results provide essential basic information for the development of gastric drug delivery systems.

Cyclooxygenase-2 mRNA expression in equine nonglandular and glandular gastric mucosal biopsy specimens obtained before and after induction of gastric ulceration via intermittent feed deprivation

To measure the expression of cyclooxygenase-2 (COX-2) mRNA in gastric biopsy specimens serially obtained from horses before, during, and after an 8-day intermittent feed-deprivation trial and to investigate the mucosal location of COX-2. 9 mixed-breed horses for retrieval of gastric biopsy specimens and 16 additional horses for immunohistochemical analysis. Gastric biopsy specimens were obtained from 6 horses; 3 of these horses and 3 more participated in an intermittent feed-deprivation trial 9 weeks later. A quantitative PCR assay was used to determine the amount of COX-2 mRNA in biopsy specimens from nonulcerated and ulcerated gastric mucosa. Immunohistochemical staining of specimens by use of a polyclonal anti-COX-2 antibody was performed on full-thickness postmortem gastric biopsy specimens. COX-2 mRNA was expressed in all glandular gastric mucosal specimens but was only detectable in nonglandular mucosal specimens when ulceration was present or during ulcer healing. Positive staining for COX-2 was present in 12 of 14 nonulcerated glandular mucosal sections. Although such staining was weak or absent in nonulcerated nonglandular sections, stronger staining was evident in regenerating epithelium at the rims of erosions and ulcers. COX-2 was constitutively present in equine glandular gastric mucosa, although its contribution to mucosal protection remains unclear. Our finding of COX-2 mRNA expression in ulcer margins during healing may support a role for the products of this enzyme in mucosal repair. The potential roles of COX-2 should be considered when COX-2-selective inhibitors are prescribed for horses with gastric ulcers.

Validation of a transendoscopic glandular and nonglandular gastric biopsy technique in horses

In order to study the evolution of histopathological and immunohistochemical changes in the gastric mucosa of horses with EGUS (equine gastric ulcer syndrome), a feasible, useful, valid and safe in vivo gastric biopsy technique is required. To determine the average gastric mucosal healing time following endoscopic gastric biopsy sampling, and evaluate the feasibility, safety and usefulness of samples obtained by this method for histopathological analysis. Six mature mares from the Faculté de Médecine Vétérinaire research herd were used. Transendoscopic gastric biopsy was performed on Days 0 and 9 using a flexible forceps with oval and fenestrated jaws to obtain gastric mucosal samples from 4 different sites: cardia (C), fundus (F), margo plicatus (MP) and glandular mucosa (GL). A maximum of 4 samples per site was taken and processed routinely for histopathology, evaluated by a pathologist. On Days 1-4 and 9-11 the lesions created by the biopsies were evaluated by gastroscopy. Lesions were evaluated over time based on a score from 0-4, where 4 was the most severe. Biopsy samples could be obtained from all targeted sites except C. No abnormal clinical signs were observed up to 7 days post biopsy. The average biopsy lesion scores decreased significantly with time for all sites. The average lesion score was significantly higher for the MP compared to the other sites at Days 1 and 2. Samples taken from the nonglandular portion of the stomach were considered inadequate for histopathology, while those taken from the glandular mucosa were adequate. The transendoscopic gastric biopsy technique described here is a feasible, safe and useful technique for obtaining samples from the equine gastric glandular mucosa. Although biopsy samples could be obtained from several areas in the nonglandular mucosa, these were very small, took longer to heal and were not considered adequate for histopathological evaluation, and another technique should therefore be validated.

Cytoprotective Effect of UlGen, a Polyherbal Formulation against Physical and Chemical Factor Induced Gastric Ulcers in Wister Albino Rats

Problem statement: UlGen, a Polyherbal formulation, was investigated for its possible Ulcero-protective activity in ulcerogen and Cold-restraint stress induced Wister rats (Rattus rattus). Oral administration of UlGen, at a dose of 800 mg kg-1 significantly protected the onset of cold-resistance stress induced ulcerations. Approach: It significantly inhibited gastric ulceration induced by alcohol and aspirin. Control group: Alcohol 80% induced ulcer was 42.00±2.30 and in UlGen treated rats showed 10.00±1.62. Using alcian blue stain to study the mucus secretion by mucosal cells carried out histological examination of gastric glandular mucosa. Results: The volume and acidity of gastric juice in pyloric-ligated rats was reduced in treated rats. Gastric volume (mL 100 g-1) in control rats showed 4.12±0.32 and in UlGen treated rats showed 2.50±0.20. Conclusion: UlGen, Cytoprotective effect may be due to the enhancement of defensive mechanism through an improvement of gastric cytoprotection as well as acid inhibition.