Malvidin Protects against and Repairs Peptic Ulcers in Mice by Alleviating Oxidative Stress and Inflammation.

Peptic ulcer episodes cause damage to the stomach and intestine, with inflammatory cell infiltration and oxidative stress as the main players. In this study, we investigated the potential of anthocyanidin malvidin for preventive and curative peptic ulcer treatment. The anthocyanidin effects were examined in gastric ulcer mouse models induced by ethanol, non-steroidal anti-inflammatory drugs (NSAIDs), ischemia-reperfusion (IR), acetic acid and duodenal ulcer induced by polypharmacy. Expression levels of oxidative and inflammatory genes were measured to investigate the mechanism of anthocyanin activity. At a dose of 5 mg·kg-1, Malvidin prevented gastric ulcer induction by ethanol, NSAID and repaired the tissue after 6 days of IR. Moreover, the anthocyanidin accelerated the healing of acetic acid-induced ulcer, increased the gene expression of EGF and COX-1, and downregulated MMP-9. Anthocyanin treatment mitigated the effect of polypharmacy on inflammation and oxidative stress observed in the intestine. Additionally, the compound downregulated cytokine expression and TLR4 and upregulated HMOX-1 and IL-10, exhibiting protective activity in the mouse gut. Malvidin thus prevented gastric and duodenal ulcers due to prominent anti-inflammatory and antioxidative effects on the gastrointestinal tract that were related to gene expression modulation and an increase in endogenous defense mechanisms.

The crosstalk between H. pylori virulence factors and the PD1:PD-L1 immune checkpoint inhibitors in progression to gastric cancer.

BACKGROUND: The progression to gastric cancer has been linked to chronic infection with Helicobacter pylori (H. pylori). Immune checkpoint inhibitors (programmed cell death -1, PD-1; programmed cell death -ligand 1, PD-L1) have a role in cancer immune escape. The relationship between H. pylori virulence factors with PD-1, PD-L1 T helper 1 (Th1), T helper 17 (Th17), and regulatory T cell (Treg) response genes, has not been thoroughly investigated in the development of gastric cancer. Therefore, we evaluated how H. pylori virulence factors influence the expression levels of immune-related genes in the development of gastric immunopathology. METHODS: A total of 92 gastric tissues of normal controls and patients with gastritis, gastric ulcer, and gastric cancer were examined for the expression of immune-checkpoint inhibitor genes (PD-1 PD-L1), Th1 (interferon- γ, IFN-γ), Th17 (interleukin- 17, IL-17, Retinoic-acid-receptor- related orphan nuclear receptor gamma t, RORγ-t), and Treg (Forkhead box P3, FOXP3) response genes with quantitative real-time PCR (qRT-PCR). Furthermore, correlation of H. pylori virulence factors' (cytotoxin-associated gene A, cagA; vacuolating cytotoxin gene A, vacA (s1,s2,m1,m2); blood group antigen-binding adhesin gene A, babA, duodenal ulcer promoting gene A, dupA; the putative neuraminyllactose-binding hemagglutinin homolog, hpaA; neutrophil-activating protein A napA; outer inflammatory protein A, oipA; urease A, ureA; and urease B, ureB) genotypes with a degree of inflammation and density of H. pylori were investigated. Next, the relationship between H. pylori virulence factors and immune-checkpoint inhibitor genes, and T-cell response genes was evaluated. Eventually, a decision tree model was developed to determine the clinical outcome of patients using expression data. RESULTS: The intensity of PD-1 and PD-L1 mRNA expression was increased significantly in gastric tissue of patients with gastric ulcer (PD-1: 2.3 fold, p=0.01; PD-L1: 2.1 fold, p=0.004), and gastric cancer (PD-1: 2 fold, p= 0.04; PD-L1: 1.8 fold, p=0.05) compared with control subjects. Also, PD-1: PD-L1 expression was significantly higher in patients with gastritis, who were infected with a marked density of H. pylori compared with its mildly infected counterparts. Furthermore, a novel negative correlation was found between PD-1 (r= -0.43) and PD-L1 (r= -0.42) with FOXP3 in patients with gastritis. CagA-positive H. pylori strain's negative association with PD-L1 expression (r=-0.34) was detected in patients with gastritis. Interestingly, PD-1 mRNA expression correlated positively with vacA s2/m2, in gastritis (r=0.43) and ulcer (r=0.43) patients. Furthermore, PD-1: PDL1 expression negatively correlated with vacA m1/m2 (r=-0.43 for PD-1; r=-0.38 for PD-L1) in gastritis patients. Moreover, an inverse correlation of PDL1 was present with vacA m1 (r=0.52) and vacA s1/m1 (r=0.46) versus vacA m2 (r=-0.44) and vacA m1 (r=0.52) and vacA s1/m2 (r=-0.14) in ulcer patients, respectively. Also, a correlation of vacA m2 (r=-0.47) and vacA s1/s2 (r= 0.45) with PD-1 was detected in ulcer patients. In addition, a novel negative correlation between FOXP3 mRNA levels and napA was shown in patients with gastritis and ulcer (r=-0.59). Finally, a computer-based model that was developed showed that knowing the expression levels of PD-L1, RORγ-t, and vacA s1/m2 would be useful to detect the clinical outcome of a patient. CONCLUSION: Our results suggested that PD-1:PD-L1 immune checkpoint inhibitors were increased in gastric pre-cancerous lesions that progress to gastric cancer. Herein, we report the relationship between H. pylori virulence factors and expression of host immune checkpoint inhibitors for diagnostic prediction of gastric malignancies using computer-based models.

Glycopeptides from Paecilomyces sinensis ameliorate ethanol-induced gastric ulcers via anti-inflammation and the miR-9-5p-MEK/ERK signaling pathway.

The aim of this study was to investigate the immunomodulatory effect and mechanism of the glycopeptides from Paecilomyces sinensis (CPS-II) on ethanol induced ulcers in mice. In this study, histopathological evaluation (H&E staining) and the gastric ulcer score, ulcer index, total acid secretion and gastric pH value were used to determine the anti-ulcer activity. The expression levels of interleukin (IL)-6, interleukin (IL)-10 and tumor necrosis factor-α (TNF-α) were detected by ELISA. The contents of superoxide dismutase (SOD), malondialdehyde (MDA) and epidermal growth factor (PEG2) in serum were measured according to the instructions for the reagents. Western blotting was used to detect the effect of CPS-II on the MEK/ERK pathway. The results showed that CPS-II could inhibit the ulcer score and ulcer index compared with the disease control group. CPS-II could significantly increase gastric pH and decrease gastric acid secretion in mice. The ELISA analysis showed that the expression levels of IL-6 and TNF-α in the CPS-II treatment group were significantly decreased, while the expression levels of IL-10 were significantly increased in the CPS-II treatment group. In the resveratrol treatment group, the content of MDA in serum was decreased, and the level of PEG2 and the activity of SOD in serum were significantly increased, which indicated that CPS-II has immunoregulation and anti-ulcer properties. The CPS-II treatment group could reduce the expression level of miR-9-5p in gastric tissue. pEGFR had been identified as a potential target of miR-9-5p. Western blot analysis showed that CPS-II could up-regulate the relative protein expression of pEGFR/EGFR, pRaf/Raf, pMEK/MEK, pERK/ERK, and ZO-1. The results showed that CPS-II could reduce oxidative stress and inflammatory response by regulating the miR-9-5p-MEK/ERK signaling pathway, thus protecting the gastric mucosa and improving stress gastric ulcers.

Efficacy of extract from Ononis spinosa L. on ethanol-induced gastric ulcer in rats.

OBJECTIVE: To investigate the efficacy of the extract from Ononis spinosa L. (O. spinosa) on ethanol-induced gastric ulcer in rats. METHODS: Phytochemical constituents of the extract from O. spinosa were analyzed using liquid chromatography-mass spectrometry. Rats were classified into 4 equal groups; ulcer control received oral vehicle; positive control was administered with 40 mg/kg esomeprazole (standard drug) and 2 groups received 0.5 and 1 g/kg of O. spinosa extract, respectively. Gastric ulcer was induced by absolute ethanol (5 mL/kg) orally to all groups. Measurement of ulcer index, cyclooxygenase-2 (COX-2) expression and determination of total glutathione level in gastric mucosa were performed. RESULTS: Oral administration of the extract from O. spinosa at doses 0.5 and 1 g/kg lowered the ulcer indices by 80.39% and 98.71% , respectively, compared to 67.89% by esomeprazole (40 mg/kg). Histologically, treatment with the extract decreased necrosis and hemorrhage in mucosa and edema and infiltration by inflammatory cells in submucosa. Using immunohistochemical technique, it was demonstrated that COX-2 expression increased in mucosa of animals treated with the extract as well as by esomeprazole. O. spinosa and esomeprazole increased total glutathione level in the stomach compared to control. Ononin was the major compound of the extract followed by trifolirhizin, myricitrin, gentisic acid, cycloartenol and quercetin. CONCLUSION: The present study demonstrated that the extract from O. spinosa was able to protect gastric mucosa from ethanol injury by at least 2 mechanisms, namely the induction of COX-2 and decreasing oxidative stress in the stomach.

Gastric Ulceration and Immune Suppression in Weaned Piglets Associated with Feed-Borne Bacillus cereus and Aspergillus fumigatus.

As a multifactorial cause, gastric ulceration-mediated diarrhea is widely prevalent in the weaned piglets, impairing pig health and economic benefits. With full implementation of antibiotic stewardship programs in China, Bacillus cereus (B. cereus) and Aspergillus fumigatus (A. fumigatus) were identified frequently in porcine feedstuffs and feeds of the animal industry. Association between feed-borne B. cereus and frequent diarrhea remains unclear. In the present study, we conducted a survey of B. cereus and A. fumigatus from feeds and feedstuffs in pig farms during hot season. Interestingly, B. cereus, B. subtilis, B. licheniformis and B. thuringinesis were isolated and identified from piglets' starter meals to sow feeds, accounting for 56.1%, 23.7%, 13.7% and 6.5%, respectively. Obviously, both B. cereus and B. subtili were dominant contaminants in the survey. In an in vitro study, Deoxynivalenol (DON) contents were determined in a dose-dependent manner post fermentation with B. cereus (405 and DawuC). Subsequently, 36 weaned piglets were randomly assigned to four groups and the piglets simultaneously received the combination of virulent B. cereus (Dawu C) and A. fumigatus while animals were inoculated with B. cereus (Dawu C), A. fumigatus or PBS as the control group. Clinically, piglets developed yellow diarrhea on day 5 and significant reductions of relative body weight were observed in the B. cereus group, and co-infection group. More importantly, IgG titers against Classical swine fever virus (CSFV) and Porcine epidemic diarrhea (PED) were reduced dramatically during 14-day observation in co-infection group, the B. cereus (Dawu C) group or the A. fumigatus group. However, lower Foot and mouth disease (FMD) -specific antibodies were reduced on day 7 compared to those of the control group. Additionally, lower lymphocyte proliferations were found in the B. cereus group and the co-infection group compared to the control group. Postmortem, higher lesions of gastric ulceration were observed in the B. cereus group and the co-infection group from day 7 to day 14 compared with those of the A. fumigatus group and the control group. Compared to the A. fumigatus group, higher DON contents were detected in the stomach inoculated with B. cereus and the co-infection with A. fumigatus. In conclusion, our data support the hypothesis that B. cereus might be associated with severe diarrhea by inducing gastric ulcerations and A. fumigatus might aggravate immune suppression, threating a sustainable swine industry. It is urgently needed to control feed-borne B. cereus contamination.

Estragole prevents gastric ulcers via cytoprotective, antioxidant and immunoregulatory mechanisms in animal models.

BACKGROUND: Estragole is an aromatic organic compound belonging to the class of phenylpropanoids derived from cinnamic aldehydes and present in essential oils of plant species, such asRavensara anisata (madeira), Ocimum basilicum (manjericão/alfavaca) and Croton zehntneri (canelinha). Pharmacological studies report its anti-inflammatory, antioxidant and vasorelaxant activity. HYPOTHESIS/PURPOSE: This study aimed to evaluate the acute non-clinical toxicity, gastroprotective activity and the related mechanisms of action. METHODS: Acute toxicity was assessed according to OECD guide 423 in mice. Ethanol, stress, piroxicam and pylorus ligation-induced gastric ulcer models were used to investigate antiulcer properties. The related mechanisms of action were using the ethanol-gastric lesions protocol. RESULTS: In the acute oral toxicity assay, doses of 300 or 2000 mg/kg of estragole administered orally in Swiss mice did not induce any behavioral changes. However, the dose of 2000 mg/kg showed a decrease in water and feed intake. Lethal dose 50 % (LD50) was set to be equal to or greater than 2500 mg/kg, according to OECD. In all evaluated protocols, estragole (31.25, 62.5, 125 and 250 mg/kg) significantly reduced the area of ​​ulcerative lesion when compared to control groups. To investigate the mechanisms involved in the gastroprotective activity, the antisecretory or neutralizing of gastric secretion, cytoprotectant, antioxidant and immunoregulatory effects were evaluated. Results showed that treatment with estragole (250 mg/kg) reduced (p < 0.05) the volume of the gastric juice. Besides, sulfhydryl groups, nitric oxide, mucus and prostaglandins seems to be involved in the gastroprotective property. Treatment also increased (p < 0.001) levels of reduced glutathione (GSH), interleukin-10 (IL-10) and positive cells marked for glutathione peroxidase (GPx) and cyclooxygenase 2 (COX-2). It also reduced (p < 0.001) malondialdehyde (MDA), myeloperoxidase (MPO), interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α) and inducible nitric oxide synthase (iNOS) (p < 0.05) levels. CONCLUSION: Thus, it is possible to infer that estragole presents gastroprotective activity related to antisecretory, cytoprotective, antioxidant and immunomodulatory mechanisms.

Rosmarinic acid prevents gastric ulcers via sulfhydryl groups reinforcement, antioxidant and immunomodulatory effects.

Rosmarinic acid (RA) is a secondary metabolite present in several plant species that has already demonstrated antioxidant, antiallergic, anticancer, antimicrobial, neuroprotective, and hepatoprotective effects experimentally. Due to the promising pharmacological properties found previously, this study aimed to assess the oral acute toxicity and the gastroprotective effect of RA using animal models. Acute toxicity was assessed according to OECD guide 423. Ethanol, stress, NSAIDs, and pylorus ligature-induced gastric ulcer models were used to investigate antiulcer properties. The related mechanisms of action were also evaluated from ethanol-induced gastric lesions protocol. RA (300 and 2000 mg/kg) showed no changes in behavioral, water and food intake, body and organs weight parameters with LD50 set around 2500 mg/kg. RA presented gastroprotective activity in all assessed doses (25, 50, 100, and 200 mg/kg) using different animal models. Besides, it was observed that this effect is not related to the modulation of gastric juice parameters (pH, volume, and [H+]), the participation of nitric oxide, mucus, and prostaglandins. However, increased sulfhydryl groups, GSH and IL-10 levels as well as reduced of proinflammatory cytokine (TNF-α and IL-1ß) levels were found for RA-treated groups. RA presents low acute toxicity and gastroprotective activity, preventing ulcer formation via cytoprotective, antioxidant, and anti-inflammatory mechanisms. Graphical abstract.

Protective effects of genipin on ethanol-induced acute gastric injury in mice by inhibiting NLRP3 inflammasome activation.

Genipin has been shown to exert anti-inflammatory effects, but its mechanism in protecting the ethanol-induced acute gastric injuries remains largely unclear. The present study aimed to investigate the effects of genipin on ethanol-induced acute gastric injuries in mice. After intragastrical administration of genipin for 7 consecutive days, acute gastric injuries were induced in the mice by ethanol treatment for 1 h. The expression levels of MDA, MPO, SOD, CAT, and NO in gastric tissues, and the levels of IL-6, TNF-α, MTL, SP, VIP and SS in serum samples were measured by ELISA. In addition, Western blotting was used to determine the expression levels of proteins involved in NLRP3 signaling pathway. The findings revealed that oral administration of genipin significantly ameliorated the pathological injury of gastric mucosa induced by ethanol, decreased the oxidative stress induced by ethanol and suppressed the expression levels of in-flammatory cytokines in gastric tissues and serum samples. In addition, it was observed that oral administration of genipin could remarkably inhibit the expression levels of related proteins in the NLRP3 signaling pathway. In conclusion, these results suggest that genipin may exhibit protective roles in ethanol-induced gastric mucosal injuries by activating antioxidant system and attenuating inflammatory reaction.

The protective role of Ocimum basilicum L. (Basil) against aspirin-induced gastric ulcer in mice: Impact on oxidative stress, inflammation, motor deficits and anxiety-like behavior.

The gastroprotective effect of Ocimum basilicum L. (Basil) hexane extract (OBHE) in aspirin-induced gastric ulcers in mice and its ameliorative effect on behavioral alterations were determined. Pretreatment with OBHE (100 or 200 mg kg-1) or misoprostol (50 µg kg-1) alleviated the aspirin-induced oxidative stress by significantly decreasing (p < 0.001) gastric ulcer index scores (57, 76 and 79%), gastric TBARS (by 49, 51 and 52%), NO (21, 28 and 29%), H2O2 (24, 42 and 45%), and the serum pro-inflammatory mediator TNF-α (21, 53 and 53%) and IL-6 (29, 30 and 31%), as well as by markedly increasing gastric GSH (41, 61 and 70%), GSH-Px (21, 32 and 34%), GST (33, 63 and 70%), GR (90, 99 and 112%), CAT (167, 211 and 267%) and serum PGE-2 levels (22, 135 and 200%) and IL-4 (64, 81 and 104%), respectively, compared with the aspirin-treated group. Meanwhile, OBHE and misoprostol induced a significant decrease (p < 0.001) in the freezing time (53, 56 and 64%), and the grooming time (by 25, 43 and 44%), respectively, compared to the aspirin treated group. This study provides evidence that OBHE confers anxiolytic, antioxidant and anti-inflammatory prophylactic effects on aspirin-induced gastric ulcers. GC/MS was used for the characterization of OBHE components. Based on the findings of this study, basil may be used as a nutritional supplement or therapeutic drug to protect against aspirin-induced gastric ulcers, a common problem resulting from the use of aspirin.

Accelerated gastric ulcer healing in thyroxine-treated rats: roles of gastric acid, mucus, and inflammatory response.

The roles of gastric acid, mucus, and inflammation on the pro-ulcer-healing effect of thyroid hormone were investigated. Male Wistar rats were randomly divided into four groups: control, thyroidectomised, thyroidectomised with thyroxine treatment (100 µg·kg-1·day-1), and sham-operated animals treated with thyroxine. Thirty-five days after thyroidectomy, sham surgery, or thyroxine treatment, an ulcer was experimentally induced. Healing was assessed 3, 7, and 10 days post-ulceration by measurement of the ulcer area, gastric mucus and acid secretion, and neutrophil lymphocyte ratio (NLR) as an index of inflammation. By day 10, the ulcer area had decreased in all groups. Recovery was significantly greater (P < 0.05) in thyroxine-treated rats (78.5% ± 1.6% reduction in ulcer area) than in controls (72.3% ± 1.2% reduction) or thyroidectomised rats (63.3% ± 1.9% reduction). Thyroxine-treated animals also had the highest reduction in NLR (65.0% ± 2.5%). Mucus secretion was significantly lower (P < 0.05) in thyroidectomised rats by days 3 and 7. Furthermore, by day 10, the concentration of basal acid decreased by 77.4% ± 2.6% in thyroxine-treated, 65.0% ± 0.0% in control, and 51.5% ± 3.3% in thyroidectomised rats. We conclude that thyroxine accelerates gastric ulcer healing by altering mucus and acid secretion and reducing NLR.

Anti-arthritic and gastroprotective activities of Ardisia crispa root partially mediated via its antioxidant effect.

Background Ardisia crispa Thunb A.DC (Myrsinaceae), commonly known as "hen's eyes", has been traditionally used in treating various inflammatory diseases. The present study evaluated anti-arthritic, gastroprotective and antioxidant activities of Ardisia crispa root hexane extract (ACRH) in various animal models. Methods Anti-arthritic activity was evaluated in complete Freund adjuvant (CFA)-induced adjuvant arthritis and gastroprotective effect was studied in the ethanol-induced ulcer model in rats. ACRH was further isolated to yield quinone-rich fraction (QRF) and both were analyzed for their total phenolic content, total flavonoid content and antioxidant activities in various antioxidant assays. Both ACRH and QRF were also analyzed for the quinone composition via gas chromatography analysis. Results ACRH exerted significant reduction of IL-1ß and TNF-α at a lower dose range in CFA-induced arthritis, as well as exhibited its cytoprotective effect against ethanol-induced ulcer lesion via involvement of mucosal nonprotein sulfhydryl (NP-SH) groups. ACRH also showed higher phenolic and flavonoid contents, as well as better antioxidant activities than QRF. Conclusions These findings demonstrated the plant as a potential anti-inflammatory agent, with ACRH succeeded in inhibiting both arthritic and ulcerogenic effect, possibly mediated via its antioxidant effect.

The Human Stomach in Health and Disease: Infection Strategies by Helicobacter pylori.

Helicobacter pylori is a bacterial pathogen which commonly colonizes the human gastric mucosa from early childhood and persists throughout life. In the vast majority of cases, the infection is asymptomatic. H. pylori is the leading cause of peptic ulcer disease and gastric cancer, however, and these outcomes occur in 10-15% of those infected. Gastric adenocarcinoma is the third most common cause of cancer-associated death, and peptic ulcer disease is a significant cause of morbidity. Disease risk is related to the interplay of numerous bacterial host and environmental factors, many of which influence chronic inflammation and damage to the gastric mucosa. This chapter summarizes what is known about health and disease in H. pylori infection, and highlights the need for additional research in this area.

Gastroprotective activity of the hydroethanolic extract and ethyl acetate fraction from Kalanchoe pinnata (Lam. ) Pers

ABSTRACT Peptic ulcers are an important pathology, and the search for safer and more effective treatment methods is of paramount importance. In this study, we assess the gastroprotective effects of the hydroethanolic extract (HE) and ethyl acetate fraction (EAF) from Kalanchoe pinnata leaves against an ethanol/HCl-induced ulcer model in rats. The HE reduced gastric lesions by approximately 47% (400 mg/kg). A significant inhibition of the gastric lesions by 50% was observed after pretreatment with the EAF (200 mg/kg). Quercetrin and quercetin 3-O-α-L-arabinopyranosyl-(1→2)-α-L-rhamnopyranoside were isolated and identified in the flavonoid fraction (EAF) by HPLC and NMR analyses because this fraction showed the highest gastroprotective effect. This fraction demonstrated high antioxidant activities (CE50=41.91 µg/mL) by DPPH in comparison with Trolox(r) and 11.33 mmol Trolox(r) equivalent by ORAC. In conclusion, the HE and FAE from K. pinnata displayed gastroprotective activity in rats, most likely due to the presence of flavonoids.

[SYSTEMIC CYTOKINOTHERAPY, USING BETALEUKIN IN A COMPLEX TREATMENT OF AN ACUTE GASTRODUODENAL ULCER BLEEDING].

Results of surgical treatment for an acute ulcer gastroduodenal bleeding in 120 patients, ageing 16-75 yrs old, were analyzed. In 20 of them a gastric ulcer was a cause of bleeding, while in 84--a duodenal ulcer, and in 16--a coexistent gastroduodenal ulcer. The bleeding activity was estimated in accordance to J. Forrest classification. In 57 patients (a comparison group) preoperatively and postoperatively a complex of a standard basal conservative therapy without immunocorrection was conducted, and in 63 (the main group)--a systemic cytokinotherapy (SCKTH), using betaleukin, was applied postoperatively additionally in a complex of therapy. A content of CD3+, CD4+, CD8+, CD19+, IgA, IgM, IgG was estimated in dynamics, as well as circulating immune complexes, phagocytic index, phagocytic number. There was established, that a dysbalance depth in the immune status have had depended upon the blood loss severity. The SCKTH application is pathogenetically substantiated, it promotes the immune status normalization, as well as a more favorable course of postoperative period and the results of treatment improvement.

[CLINICAL AND ENDOSCOPIC, MORPHOLOGIC AND IMMUNOHISTOCHEMICAL FEATURES OF GASTRIC ULCER IN H. PYLORI-INFECTED INDIVIDUALS RECEIVING CYTOTOXIC THERAPY].

THE PURPOSE OF THE STUDY: To determine the prognostic significance of the expression of molecules of PCNA, Bcl-2, NF-Kb and tachykinins (substance P, neurokinin A) in patients with gastric ulcer (CU) receiving cytotoxic therapy. MATERIALS AND METHODS: Total surveyed 90 patients divided into 3. equal groups. The first comparison group consisted of patients with chronic atrophic H. pylori-associated gastritis (CAG) (30 pers.). A second control group consisted of patients with gastric ulcer (30 pers.). Third, the study group consisted of 30 people. with CU suffering from hematological malignancies, in a period of complete clinical remission of the disease and receiving supportive polychemotherapy (PCT). Patients underwent endoscopy, morphological and immunohistochemical study of the mucous membrane of the antrum and body of the stomach to detect the expression of molecules of PCNA, Bcl-2, neurokinin A, substance P and factor Nf-Kb. RESULTS: The total level of dyspeptic syndrome on visual scale analogue in patients receiving chemotherapy and GU (GUpct) was significantly higher (p < 0.05) compared with patients with GU. It should be noted that patients with GUpct reducing clinical symptoms is much slower (p < 0.05). At the same time in 13 (43.3%) patients with GUpct determines the duration of ulcer healing, whereas in patients with GU in only 4 (13.3%) patients. Patients with GUpct more frequently (p < 0.05) were verified II and stage Ill chronic gastritis (CG), while Stage I--less (p < 0.05). Patients with GUpct significantly more often (p<0.05) was determined by the II degree of CG and significantly less (p < 0.05)--IV degree. Patients with GUpct determined significantly lower (p < 0.05), the expression performance PCNA, substance P and neurokinin A and higher (p < 0.05)--Bcl-2 and factor Nf-kB. CONCLUSION: GU in patients receiving chemotherapy, dyspeptic syndrome is characterized by severe, advanced stage of CG on the background of relatively low severity of CG in accordance with the classification of OLGA (2008). Patients with GUpht have a significant level of violation of regeneration changes how is this atrophy, intestinal metaplasia, dysplasia of gastric mucosa association with gross violations of the processes of epithelial cell homeostasis of epithelial cells regulation after molecules PCNA, Bcl-2, NF-kB and tachykinins (substation P, neurokinin A).

[CMV-associated gastric ulcer in an immunocompetent male patient]. / CMV-assoziiertes Ulcus ventriculi bei einem immunkompetenten Patienten.

This article reports the case of a 45-year-old male immunocompetent patient who presented with acute epigastric pain and vomiting. Diagnostic tests confirmed a recent cytomegalovirus (CMV) infection as a contributory cause of a florid gastric ulcer. Primary CMV infections affecting the upper gastrointestinal tract are rare in immunocompetent adults. In this case treatment with a proton pump inhibitor and eradication of concomitant Helicobacter pylori colonization led to a full recovery. Anti-CMV treatment was not necessary.

Serotonin and histamine mediate gastroprotective effect of fluoxetine against experimentally-induced ulcers in rats.

Research in the treatment of gastric ulcer has involved the investigation of new alternatives, such as anti-depressant drugs. The present study was designed to investigate the gastroprotective effects of fluoxetine against indomethacin and alcohol induced gastric ulcers in rats and the potential mechanisms of that effect. Fluoxetine (20 mg/kg) was administered IP for 14 days. For comparative purposes, other rats were treated with ranitidine (30 mg/kg). Thereafter, after 24 h of fasting, INDO (100 mg/kg) or absolute alcohol (5 ml/kg) was administered to all rats (saline was administered to naïve controls) and rats in each group were sacrificed 5 h (for INDO rats) or 1 h (for alcohol rats) later. Macroscopic examination revealed that both fluoxetine and ranitidine decreased ulcer scores in variable ratios, which was supported by microscopic histopathological examination. Biochemical analysis of fluoxetine- or ranitidine-pre-treated host tissues demonstrated reductions in tumor necrosis factor (TNF)-α and myeloperoxidase (MPO) levels and concomitant increases in gastric pH, nitric oxide (NO) and reduced glutathione (GSH) contents. Fluoxetine, more than ranitidine, also resulted in serotonin and histamine levels nearest to control values. Moreover, immuno-histochemical analysis showed that fluoxetine markedly enhanced expression of cyclo-oxygenases COX-1 and COX-2 in both models; in comparison, ranitidine did not affect COX-1 expression in either ulcer model but caused moderate increases in COX-2 expression in INDO-induced hosts and high expression in alcohol-induced hosts. The results here indicated fluoxetine exhibited better gastroprotective effects than ranitidine and this could be due to anti-secretory, anti-oxidant, anti-inflammatory and anti-histaminic effects of the drug, as well as a stabilization of gastric serotonin levels.