Gastric Mucosal Lesions Research Articles

Mucosal lesions of the upper gastrointestinal tract in patients with ulcerative colitis: A review.

Ulcerative colitis (UC) is a chronic, nonspecific, relapsing inflammatory bowel disease. The colorectum is considered the chief target organ of UC, whereas upper gastrointestinal (UGI) tract manifestations are infrequent. Recently, emerging evidence has suggested that UC presents complications in esophageal, stomachic, and duodenal mucosal injuries. However, UC-related UGI tract manifestations are varied and frequently silenced or concealed. Moreover, the endoscopic and microscopic characteristics of UGI tract complicated with UC are nonspecific. Therefore, UGI involvement may be ignored by many clinicians. In addition, no standard criteria have been established for patients with UC who should undergo fibrogastroduodenoscopy. Furthermore, specific treatment recommendations may be needed for patients with UC-associated UGI lesions. Herein, we review the esophageal, gastric, and duodenal mucosal lesions of the UC-associated UGI tract, as well as the potential pathogenesis and therapy.

Effect of a Cytoprotective Dose of Dehydroleucodine, Xanthatin, and 3-Benzyloxymethyl-5H-furan-2-one on Gastric Mucosal Lesions Induced by Mast Cell Activation.

The aim of this study was to determine whether the lactones dehydroleucodine, xanthatin and 3-benzyloxymethyl-5H-furan-2-one, would be effective in an animal model of gastric ulcer induced by mast cell activation. Rats were divided into ten groups. Treatments were repeated for four days. The degree of gastric erosion was assessed with a scoring system and histological preparations. Gastric mast cell morphology was analyzed by histological procedures. Serum serotonin levels were determined as markers of mast cell activation. Statistical analyses were done using ANOVA and Tukey–Kramer test. We demonstrated that the repeated administration of compound 48/80 results in extensive mucosal lesions in the gastric mucosa and that such lesions occurred in association with mast cell degranulation and a significant increase of serum serotonin. We showed that these lesions were prevented by dehydroleucodine, xanthatin, and 3-benzyloxymethyl-5H-furan-2-one and that this effect was similar to that obtained with sodium cromoglycate. In conclusion, the results of the present study indicate that the optimal gastric cytoprotective dose of dehydroleucodine, xanthatin, and 3-benzyloxymethyl-5H-furan-2-one is efficacious in an animal model of gastric ulcer induced by mast cell activation. Our findings suggest that these lactones could be valuable tools for designing novel therapeutic agents for digestive disorders associated with inappropriate mast cell activation.

Effects of complex extracts of traditional Chinese herbs on gastric mucosal injury in rats and potential underlying mechanism

AbstractFive complex extracts (CEs) of seven Chinese herbs (Astragalus, Poria cocos, Alpinia officinarum Hance, Radix Puerariae, Ginseng, Licorice, Hericium erinaceus) were prepared by hot water extraction and evaluated for their effect on gastric ulcer in rats. In rats with acetic acid‐induced chronic gastric ulcer, gross and microscopic appearance showed that gastric mucosal injury index and lesion inhibition rate were improved after CEs gavage for 21 days. Pretreatment with CEs for 21 days in rats with acute gastric ulcer could also improve the gastric mucosal injury by ethanol. CE1, CE4, and CE5 showed more obvious effect in two models. The cell experiments results showed that CE1, CE4, and CE5 effectively inhibited Wnt signaling activity. Thus, they could protect gastric mucosa through inhibiting Wnt signaling pathway. These results indicated that CE1, CE4, and CE5 had significant protective effects on gastric mucosal injury by inhibiting Wnt signalling pathway and could be developed into safe functional products.

136 Evaluation on the occurrence of gastritis in foals during weaning

Inflammation of the gastric mucosa, also known as gastritis, are diseases that can commonly affect foals. The hypothesis is that gastritis is present before weaning. Furthermore, foals weaned in paddocks collectively have a lower incidence of clinical gastritis compared with foals weaned individually in stalls. This study aimed to assess the occurrence of gastritis in crossbred foals submitted to 2 weaning methods. The experiment was conducted at the LabEqui, located at USP. Sixteen crossbred foals, male and female, were used, with an approximate age of 5 mo and body weight between 230 and 260 kg. During the lactation period, foals and mares were housed together in a collective paddock of 10,000 m2, without access to grass. After weaning, a group of foals was housed in individual pens, with a size of 16 m2 and a bed of wood shavings. The rest remained in the collective paddock. The experimental design used was randomized blocks. The treatments consisted of: Weaning in a paddock; Weaning in a stall. The foals were weaned abruptly (mares removed). All animals before weaning received concentrate equivalent to 0.25% of live weight in dry matter and, after weaning, 1.25% in dry matter, according to nutritional requirements. Hay, water and mineral salt were provided ad libitum. Gastric mucosal lesions were evaluated using a score for the number of lesions assessed on a scale of 0 to 4, and intensity of gastric lesions assessed on a scale of 0 to 5, through gastroscopy. The foals were evaluated once 15 d before weaning and once 15 d after weaning. The results were subjected to ANOVA and means compared by Tukey test, at 5% significance level, using the PROC MIXED procedure of SAS (9.0, Cary, NC). There was no difference (P > 0.05) between treatments for the number of gastric lesions, before weaning, with an average score of 3.00 for paddock and 1.56 for stall, as well as, after weaning, with averages of 1.75 for paddock and 1.25 for stall. However, there was a difference (P

Antiulcer Potential of Olea europea L. cv. Arbequina Leaf Extract Supported by Metabolic Profiling and Molecular Docking.

Gastric ulceration is among the most serious humanpublic health problems. Olea europea L. cv. Arbequina is one of the numerous olive varieties which have scarcely been studied. The reported antioxidant and anti-inflammatory potential of the olive plant make it a potential prophylactic natural product against gastric ulcers. Consequently, the main goal of this study is to investigate the gastroprotective effect of Olea europea L. cv. Arbequina leaf extract. LC-HRMS-based metabolic profiling of the alcoholic extract of Olea europea L. cv. Arbequina led to the dereplication of 18 putative compounds (1–18). In vivo indomethacin-induced gastric ulcer in a rat model was established and the Olea europea extract was tested at a dose of 300 mg kg−1 compared to cimetidine (100 mg kg−1). The assessment of gastric mucosal lesions and histopathology of gastric tissue was done. It has been proved that Olea europea significantly decreased the ulcer index and protected the mucosa from lesions. The antioxidant potential of the extract was evaluated using three in vitro assays, H2O2 scavenging, xanthine oxidase inhibitory, and superoxide radical scavenging activities and showed promising activities. Moreover, an in silico based study was performed on the putatively dereplicated compounds, which highlighted that 3-hydroxy tyrosol (4) and oleacein (18) can target the 5-lipoxygenase enzyme (5-LOX) as a protective mechanism against the pathogenesis of ulceration. Upon experimental validation, both compounds 3-hydroxy tyrosol (HT) and oleacein (OC) (4 and 18, respectively) exhibited a significant in vitro 5-LOX inhibitory activity with IC50 values of 8.6 and 5.8 µg/mL, respectively. The present study suggested a possible implication of O. europea leaves as a potential candidate having gastroprotective, antioxidant, and 5-LOX inhibitory activity for the management of gastric ulcers.

Dynamic observation of the progression of chronic gastritis to gastric cancer in a disease–TCM pattern rat model

To dynamically observe the progression of chronic gastritis to gastric cancer (GC) in disease-traditional Chinese medicine (TCM) pattern rats to provide data for understanding the disease progression and effective approaches for drug screening and mechanism exploration. Wistar rats were randomly divided into control (n = 96, half female and half male) and model (n = 336, half female and half male) groups. Model rats received free access to N-methyl-N′-nitro-N-nitrosoguanidine (120 μg/mL), sodium deoxycholate (20 mmol/L), and alcohol (45%), and were subjected to intermittent fasting. Mortality rate, body weight, water consumption, food intake, gastric pathology, blood content analysis, and liver and kidney function of model rats were dynamically monitored over 30 weeks. In the 30 th week, pattern characteristics were assessed. Gastric pathology and pattern characteristics were observed for an additional 8 weeks to evaluate stability. The overall mortality of the model group was 34.82% (33.10% for females and 36.55% for males) at 30 weeks post-intervention. Inflammatory cell infiltration, glandular atrophy, atypical hyperplasia, and GC manifested successively in the gastric mucosa of rats. In model rats, N-methyl-N′-nitro-N-nitrosoguanidine intake was lower in males than in females, whereas pathological changes in the gastric mucosa occurred earlier in females than in males. Notably, gastric mucosal lesions were more severe in males than in females. Our modeling methods maintained stable gastric mucosal lesions for at least 8 weeks after final intervention. The pattern characteristics observed in model rats at the 30 th and 38 th week were consistent with those of spleen deficiency, blood stasis, and yin deficiency pattern. Blood content and indexes of liver and kidney function in the model group were normal. Our findings provide evidence for the pathological stages underscoring the progression of chronic gastritis to GC in disease-TCM pattern rats, which may facilitate development of relevant pharmacotherapies.

Antiulcer and Antioxidant Potential of Eucalyptus camaldulensis Leaves Methanol Extract in Albino Rats

Aim: This research is aimed at assessing the antiulcer and antioxidant potential of Eucalyptus camaldulensis leaves methanol extract in albino rats.
 Methodology: Fresh leaves of Eucalyptus camaldulensis were harvested from the Department of Plant Science and Biotechnology, Kebbi State University of Science and Technology, Aliero. The dried pulverized leaves were extracted using Soxhlet apparatus with methanol as the solvent. Thirty male albino rats weighing between 200 g and 250 g were used in this study. The rats were randomly divided into six (6) groups of five (5) rats each. Antiulcer and antioxidant activity was evaluated using ethanol-induced ulcer model. Ulcer was induced in all groups except Group 1 which served as the control and received distilled water only. Group 2 was not treated while Group 3 was treated with omeprazole (50mg/kg). Groups 4, 5 and 6 were treated with 200mg/kg, 400mg/kg and 800mg/kg of the extract respectively. After seven days of treatment, the albino rats were humanely sacrificed, ulcer index determined and the serum assessed for antioxidants levels.
 Results: The gastric mucosal lesions produced in the untreated group were very visible and had an ulcer index of 12.83. Pre-treatment with omeprazole and graded doses of the extract showed significant reductions (P<.05) in ulcer index in a dose dependent manner. The SOD, CAT, GPx, GSH and MDA levels were significantly reduced (P<.05) in the untreated group with progressive reduction in the treated groups as the extract concentration reduced. The antioxidant vitamins (Vitamin A, C and E) reduced in concentration significantly (P<.05) without any significant difference between the untreated group and the groups that received 200mg/kg and 400mg/kg of the extract. Meanwhile, the group treated with 800mg/kg of the extract significantly increased (P<.05) the concentrations of these vitamins when compared to the group that received ethanol only.
 Conclusion: Eucalyptus camaldulensis leaves methanol extract possesses both antiulcer and antioxidant activity. This justifies the use of Eucalyptus camaldulensis leaves in traditional medicine in the management of ulcer and validates its antiulcer potential.

Protective Effect of Pyrus ussuriensis Maxim. Extract against Ethanol-Induced Gastritis in Rats.

Pyrus ussuriensis Maxim (Korean pear) has been used for hundreds of years as a traditional herbal medicine for asthma, cough, and atopic dermatitis in Korea and China. Although it was originally shown to possess anti-inflammatory, antioxidant, and antiatopic properties, its gastroprotective effects have not been investigated. In the present study, we evaluated the protective effects of Pyrus ussuriensis Maxim extract (PUE) against ethanol-induced gastritis in rats. The bioactive compound profile of PUE was determined by gas chromatography mass spectroscopy (GC-MS) and high-performance liquid chromatography (HPLC). The gastroprotection of PUE at different doses (250 and 500 mg/kg body weight) prior to ethanol ingestion was evaluated using an in vivo gastritis rat model. Several endpoints were evaluated, including gastric mucosal lesions, cellular degeneration, intracellular damage, and immunohistochemical localization of leucocyte common antigen. The gastric mucosal injury and ulcer score were determined by evaluating the inflamed gastric mucosa and by histological examination. To identify the mechanisms of gastroprotection by PUE, antisecretory action and plasma prostaglandin E2 (PGE2), gastric mucosal cyclic adenosine monophosphate (cAMP), and histamine levels were measured. PUE exhibited significant antioxidant effects with IC50 values of 56.18 and 22.49 µg/mL for 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2′- azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid (ABTS) inhibition (%), respectively. In addition, GC/MS and HPLC analyses revealed several bioactive compounds of PUE. Pretreatment with PUE significantly (p < 0.05) decreased the ulcer index by preventing gastric mucosal lesions, erosion, and cellular degeneration. An immunohistochemical analysis revealed that PUE markedly attenuated leucocyte infiltration in a dose-dependent manner. The enhancement of PGE2 levels and attenuation of cAMP levels along with the inhibition of histamine release following PUE pretreatment was associated with the cytoprotective and healing effects of PUE. In contrast, the downregulation of the H+/K+ ATPase pathway as well as muscarinic receptor (M3R) and histamine receptor (H2R) inhibition was also involved in the gastroprotective effects of PUE; however, the expression of cholecystokinin-2 receptors (CCK2R) was unchanged. Finally, no signs of toxicity were observed following PUE treatment. Based on our results, we conclude that PUE represents an effective therapeutic option to reduce the risk of gastritis and warrants further study.

Epigallocatechin Gallate Protects against MNNG-Induced Precancerous Lesions of Gastric Carcinoma in Rats via PI3K/Akt/mTOR Pathway.

Objective To evaluate the therapeutic effect of epigallocatechin gallate (EGCG) on precancerous lesions of gastric carcinoma (PLGC) and to determine whether EGCG protects against PLGC by regulating PI3K/Akt/mTOR pathway. Methods Twenty-four male Wistar rats were randomly divided into 3 groups: normal control group (NC), PLGC model group (MC), and group of PLGC rats treated with EGCG (MC + EGCG). 1-Methyl-3-nitro-1-nitrosoguanidine (MNNG) and sodium salicylate were combined and used to establish the PLGC rat animal model. The therapeutic effect of EGCG on PLGC was evaluated by body weight and pathological lesions of gastric mucosa in PLGC rats. Quantitative polymerase chain reaction (qPCR) was applied to measure the mRNA expressions of PI3K, Akt, and mTOR. The protein expressions of cleaved caspase-3, PTEN, PI3K, p-PI3K, Akt, p-Akt, p-mTOR, and mTOR were determined by automated western immunoblotting. Results The body weight decreased in PLGC rats while EGCG significantly increased body weight. The gastric mucosa of PLGC rats exhibited the pathological lesions of atrophy, intestinal metaplasia, and atypical hyperplasia while EGCG could ameliorate the pathological lesions. EGCG could upregulate the expressions of cleaved caspase-3 and PTEN and reduce the expressions of PI3K, Akt, and mTOR. Conclusions EGCG ameliorated pathological lesions of PLGC and exerted the effect of apoptosis promotion in PLGC rats. The apoptotic pathway triggered by EGCG may be related to inhibition of PI3K/Akt/mTOR pathway. It provided a theoretical basis for the PLGC treatment and gastric cancer prevention.

Short-chain fatty acid butyrate: A novel shield against chronic gastric ulcer.

Butyrate is one of the most abundant short-chain fatty acids produced by intestinal bacteria. In the present study, the action of butyrate on chronic gastric mucosa lesions was investigated, as well as its underlying mechanism in mice. Male mice from the Institute of Cancer Research were randomly divided into three groups: Sham, model and butyrate groups. Butyrate was administered intragastrically for 7 days to butyrate group mice following the establishment of a gastric ulcer model. Hematoxylin and eosin staining, immunohistochemical analysis, enzyme-linked immunosorbent assay and quantitative polymerase chain reaction were used to determine the therapeutic effects and molecular mechanism of butyrate treatment. The findings demonstrated that butyrate induced a marked shift in superoxide dismutase and catalase activities, along with a decrease in malondialdehyde levels, thereby attenuating oxidative stress. Furthermore, butyrate decreased the levels of pro-inflammatory cytokines interleukin-1β, tumour necrosis factor-α and leukotriene B4, which helped combat inflammatory responses. Moreover, butyrate treatment exerted remarkable positive influences that mediate an increase in 6-keto-PGF-1α (a degradation product of prostacyclin), trefoil factor 2, MUC5AC and fibroblast growth factor-7 levels to promote gastric mucosal repair. The expression of specific receptor GPR109A for butyrate was upregulated, with no significant difference noted in the expression of GPR43 or GPR41. Overall, the present findings revealed that butyrate exerted therapeutic effects by upregulating mucosal repair factors and stimulating protective responses against oxidation and inflammation. GPR109A may be the key receptor for butyrate therapy.

A Deep Learning Model for Diagnosing Gastric Mucosal Lesions Using Endoscopic Images: Development, Validation, and Method Comparison

Background: Endoscopic differential diagnoses of gastric mucosal lesions (benign gastric ulcer, early gastric cancer [EGC], and advanced gastric cancer) remain challenging. We aimed to develop and validate convolutional neural network-based artificial intelligence (AI) models: lesion detection (AI-LD), differential diagnosis (AI-DDx), and invasion-depth (AI-ID, pT1a vs. pT1b among EGC) models. Methods: This study included 1,366 consecutive patients with gastric mucosal lesions from two referral centers in Korea. One representative endoscopic image from each patient was used. Histological diagnoses were set as the gold standard. The performances of the AI-DDx (training/internal/external validation set, n=1009/112/245) and AI-ID (training/internal/external validation set, n=620/68/155) were compared with visual diagnoses by independent endoscopists (stratified by novice [ 5 years of experience]) in a prospective manner and by endoscopic ultrasonography (EUS), respectively. Findings: The AI-DDx showed good diagnostic performance for both internal (area under of the receiver operating characteristic curve [AUROC]=0.86) and external validation (AUROC=0.86). The performance of the AI-DDx was better than that of the novice (AUROC=0.82, P=0.01) and intermediate endoscopists (AUROC=0.84, P=0.02), but was comparable to the experts (AUROC=0.89, P=0.12) in the external validation set. The AI-ID showed fair performances in both internal (AUROC=0.78) and external validation sets (AUROC=0.73), which were significantly better than EUS results performed by experts (internal validation: AUROC=0.62, external validation: AUROC=0.56; both P <0.001). Interpretation: The AI-DDx was comparable with experts and outperformed novice and intermediate endoscopists for the differential diagnosis of gastric mucosal lesion. The AI-ID performed better than EUS for the invasion-depth evaluation. Funding Statement: Seoul National University Hospital (No. 04-2020-0860). Declaration of Interests: The authors confirm that this article content has no conflict of interest. Ethics Approval Statement: The present study was approved by the institutional review boards of the two participating institutions (IRB No.: 1706-109-859 [SNUH] and 2020-08-135 [SMC]) and conducted following the ethical guidelines of the World Medical Association Declaration of Helsinki. Informed patient consent was waived by the institutional review board of each institution owing to the retrospective nature of the study.

Low-dose PPI to prevent bleeding after ESD: A multicenter randomized controlled study

BackgroundAlthough proton pump inhibitors (PPIs) are widely used in the prevention of gastric bleeding caused by endoscopic submucosal dissection (ESD), there is no consensus on the optimal regimen for these patients. Therefore, we aim to investigate whether intermittent use of low-dose PPI is sufficient to prevent post-ESD bleeding. MethodsThis multicenter, non-inferiority, randomized controlled trial was conducted at 9 hospitals in China. Consecutive eligible patients with a diagnosis of gastric mucosal lesions after ESD treatment were randomly assigned (1:1) to receive either intermittent low-dose or continuous high-dose PPIs treatment. After three days, all patients administered orally esomeprazole 40 mg once a day for 8 weeks. The primary endpoint was post-ESD bleeding within 7 days. Analysis was done according to the intention-to-treat principle with the non-inferiority margin (Δ) of 5%. Results526 consecutive patients were assessed for eligibility from 30 September 2017 to 30 July 2019, of whom 414 were randomly assigned to low-dose (n = 209) or high-dose (n = 205) esomeprazole treatment group without dropouts within7 days. The total post-ESD bleeding is occurred in 13 (6.2 %, 95 % CI 3.3–9.6) of 209 within 7 days in the intermittent low-dose group, and 12 (5.9 %, 95 % CI 2.9–9.3) of 205 in the continuous high-dose group. The absolute risk reduction (ARR) was 0.4 % (−4.2, 4.9). One month after ESD, There are 44 patients (21.1 %, 95 % CI 15.8, 26.8) and 39 patients (19.0 % 95 % CI 13.7, 24.4) in scar stage respectively in low-dose group and high-dose group (P = 0.875).The hospital costs in the low-dose PPI group was lower than high -dose group (P = 0.005). ConclusionThe intermittent use of low-dose PPIs is sufficient to prevent post-ESD bleeding. It might be applied in clinical practice to prevent post-ESD bleeding and reduce the costs related to PPIs.

Limb Ischemic Preconditioning or Dezocine Pre-Treatment will Reduce Acute Gastric Mucosal Injury in Rats

Acute gastric mucosal lesions refer to acute inflammation of the gastric mucosa [1,2], Symptoms including gastric mucosal congestion, edema, and erosion...

New canine parvovirus 2a infection in an imported Asian small-clawed otter (Aonyx cinereus) in Japan.

Post-import from the Republic of Indonesia to Japan in 2017, two juvenile, captive bred Asian small-clawed otters (Aonyx cinereus) exhibited gastrointestinal symptoms, including vomiting, diarrhea, and hematemesis, and died. One of them was examined postmortem. Microscopically, the small intestinal mucosa was necrotic with crypts lined by regenerating large epithelial cells. A gastric cardiac mucosal ulcerative lesion containing fungal yeasts and pseudohyphae morphologically indicated Candida spp. The lymph nodes exhibited marked lymphoid depletion. Canine parvovirus 2 (CPV-2) was isolated from an oral swab, and virus protein 2 (VP2) gene sequencing revealed new CPV-2a. To our knowledge, this is the first new CPV-2a infection report in Asian small-clawed otters. This infection should be considered in gastrointestinal symptom-related cases in this species.

Effect of a novel rice fermented extract on gastric ulcers in horses.

Gastric ulcers cause appetite loss, poor body condition, and colic in horses. This study investigated the protective effect of a rice fermented extract on the gastric mucosa in 17 healthy Thoroughbreds. For one month, horses in the rice fermented extract (nine horses) and control (eight horses) groups were orally administered a rice fermented extract (100%; 0.2 ml/kg, SID) and tap water (0.2 ml/kg), respectively. Gastric endoscopic images were obtained before and one month after rice fermented extract administration. The gastric ulcer score was lower after administration (median, 1; maximum, 2; minimum, 1) than before administration (median, 4; maximum, 4; minimum, 3) in the rice fermented extract group (P<0.05). In conclusion, the administration of a rice fermented extract for one month improves gastric mucosal lesions in Thoroughbreds with gastric ulcers.

Polygonum hydropiper extract attenuates ethanol-induced gastric damage through antioxidant and anti-inflammatory pathways.

The present study was conducted to investigate the underlying mechanisms and effective components of Polygonum hydropiper in ethanol-induced acute gastric mucosal lesions. The ethanol extract was purified on an AB-8 macroporous resin column and eluted with 60% ethanol and was then injected into the HPLC system for quantitative analysis. Sprague-Dawley rats were orally pretreated with P. hydropiper extract (PHLE; 50, 100, and 200 mg/kg) for 5 days and then absolute ethanol was administered to induce gastric mucosal damage. One hour after ethanol ingestion, the rats were euthanized and stomach samples were collected for biochemical analysis. Antioxidant enzymes and anti-inflammatory cytokines were quantified. Western blotting was used to detect the expression levels of proteins. Cell proliferation was assayed by CCK-8 assays. The proportion of total flavonoids in the final extract of P. hydropiper was 50.05%, which contained three major bioactive flavonoid constituents, including rutin, quercitrin, and quercetin. PHLE significantly increased cell viability and effectively protected human gastric epithelial cells-1 against alcohol-induced damage in vitro. PHLE pretreatment attenuated gastric mucosal injuries in a dose-dependent manner in rats, and increased the activity of superoxide dismutase, glutathione peroxidase, and glutathione, and decreased the levels of malondialdehyde in gastric tissue. Pretreatment with PHLE also reduced the generation of the pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1β in gastric tissue by downregulating the expression of nuclear factor-kappa B. PHLE exerted protective effects against gastric injury through antioxidant and anti-inflammatory pathways. Flavonoids might be the main effective components of P. hydropiper against gastric mucosal injury.

IGHG1 induces EMT in gastric cancer cells by regulating TGF-β/SMAD3 signaling pathway.

Objective: Gastric cancer is one of the most common malignant tumors in the world. IGHG1 is a differentially expressed protein screened out in gastric cancer in the early stage of the subject group. This topic explores the expression of IGHG1 in gastric cancer and the effect of IGHG1 on the proliferation, migration, invasion and EMT of gastric cancer SGC7901 cells and its mechanism of action.Methods: Twenty cases of gastric cancer were purified by laser Capture Microdissection. The isotopic tags for relative and absolute quantification was used to label the proteins, and then analyzed and identified them by quantitative proteomics. Immunohistochemical staining method was used to detect the expression of IGHG1 protein in gastric cancer tissues. Western blot was used to detect the expression of IGHG1 in gastric cancer cells. The MTT and Petri dish clone formation experiment analyzed the effect of low expression of IGHG1 on the proliferation of SGC7901 cells. Scratch test and Transwell migration and invasion test to observe the effect of low expression of IGHG1 on the migration and invasion of SGC7901 cells. Western blot was used to detect the effect of low expression of IGHG1 on the expression of EMT-related proteins.Results: 243 proteins related to gastric mucosal lesions were preliminarily identified. We found that IGHG1 is highly expressed in gastric cancer tissues compared with normal control tissues. IGHG1 promotes the proliferation, migration and invasion of gastric cancer cells. Compared with the control group, the expression of EMT-related proteins Vimentin, N-cadherin, TGF-β, P-SMAD3 was decreased and the expression of E-cadherin was increased after IGHG1 low expression.Conclusions: IGHG1 induces EMT in SGC7901 cells by regulating the TGF-β/SMAD3 signaling pathway.

Protective effect of standardised fruit extract of Garcinia cowa Roxb. ex Choisy against ethanol induced gastric mucosal lesions in Wistar rats

Background and aim The fruit of Garcinia is a rich and valuable source of bioactive compounds and is traditionally used for treating wounds and ulcers. The present study was carried out to investigate the protective effect of chromatographically standardized fruit extract of Garcinia cowa (GCE) on ethanol-induced gastric lesions in rats and its possible mechanisms. Methods The effect of GCE (200 and 400 mg/kg body weight) was evaluated by determining various gastric ulcer parameters like gastric wall mucus, non-protein sulfhydryls (NP-SH) content, microvascular permeability, endogenous antioxidant enzyme, and gastric histopathological study. Results and conclusions Oral administration of GCE at doses of 200 and 400 mg/kg exhibited significant (p < .01) dose-dependent inhibition of ulcer index by 18.94–44.02%, respectively. Pre-treatment of rats with GCE (400 mg/kg) significantly restored the depleted gastric wall mucus level by 34.09% and NP-SH content by 33.35% induced by ethanol administration. In addition, GCE (400 mg/kg) showed a significant decrease in microvascular permeability of Evans Blue by 47.43%, rationalizing its protective effect. Furthermore, a significant increase in oxidative enzyme levels with reduction in malondialdehyde level and elevation of superoxide dismutase (SOD) activity was observed in the GCE treated group as compared to the ulcer control group. The histopathological assessment also confirmed the protective nature of GCE. HPTLC analysis showed the presence of 0.27%, 0.11% w/w gallic acid, and amentoflavone, respectively in GCE. The content of α-mangostin and xanthochymol in the G. cowa extract sample quantified by HPLC-PDA method was 0.72 and 8.46%, respectively. The results obtained indicate that the protective effect of GCE against gastric ulcers in rats through multiple actions confirmed by the reduction of oxidative stress and restoration of adhered gastric mucus, NP-SH content, and histological architecture. KEY MESSAGES Ethanol is the most typical ulcerogenic agent and has been shown to extend the risk of ulcer in humans. Natural products are promising alternative medication for the development of new drugs to regulate gastrointestinal diseases. Garcinia cowa protects the gastric mucosa through multiple actions that include restoration of adhered gastric mucus and inhibition of lipid peroxidation.

Cashew apple byproduct: Gastroprotective effects of standardized extract

Ethnopharmacological relevanceThe incidence of gastric mucosa lesions in the adult population has increased mainly due to the continued use of nonsteroidal anti-inflammatory drugs (NSAIDs). The cashew (Anacardium occidentale L.) is a tropical tree, cultivated in several countries, whose barks, leaves and pseudofruit (cashew apple) are popularly used in traditional medicine for the treatment of many diseases, including gastric ulcer. AimOur study evaluated the potential gastroprotective effect of the carotenoid and anacardic acids-enriched aqueous extract (CAE), prepared from cashew apple pomace, in the dose-repeated acetylsalicylic acid (ASA)-induced gastric lesions model in rats. Material and methodsAfter randomly distribution into five group (G1 – G5, n = 8 animals/group), male Wistar rats were daily treated with ASA solution (200 mg/kg, 5 ml/kg, G2 - G5) or potable water (Satellite group, G1) during 14 days. From 8th to 14th experimental day, rats in G3 - G5 groups were orally treated with CAE (50, 100 and 500 mg/kg, 5 ml/kg, respectively). Body weight was measured on 0, 7th and 14th day. On the 14th experimental day, all surviving animals were euthanized for macroscopic evaluation of the inner organs and stomach removal. After weighting, each stomach was properly prepared for biochemical analysis [myeloperoxidase activity (MPO), reduced glutathione analysis (GSH), IL-1β, CXCL2/MIP-2, TNF-α and IL-10 levels]. ResultsAt the most efficient dose (100 mg/kg, p.o.), CAE-treated animals showed a slight improvement in the macroscopic aspect of gastric mucosa associated with significant (p < 0.05) reduced levels of IL-1β, CXCL2/MIP-2, and MPO activity besides increased levels of GSH (partially), and IL-10 in stomach tissues. ConclusionsThe present study demonstrated that the carotenoid and anacardic acids-enriched extract obtained from cashew apple pomace is a promising raw material for the development of herbal medicine and/or functional food supplements for the adjuvant treatment of NSAIDs-induced gastric ulcers.

Clip band ligation ablation.

Band ligation–assisted endoscopic mucosal resection (BL-EMR) is an established procedure to remove esophageal, gastric, and rectal mucosal and submucosal lesions.1 Not infrequently, small duodenal carcinoids or neuroendocrine tumors (NETs) are found during routine endoscopy. These tumors are located in the submucosal and mucosal layers. Although there are reports of managing small duodenal NETs with BL-EMR,2 there are risks of perforation.3