scholarly journals Further observations on the pathology of gastric ulcer. (Progress report.)

1910 ◽  
Vol 82 (555) ◽  
pp. 233-248 ◽  
Keyword(s):  
Gastric Ulcer ◽  
Guinea Pig ◽  
Mucous Membrane ◽  
Mode Of Action ◽  
Progress Report ◽  
Gastric Ulcers ◽  
Gastric Cells

The gastric ulcers in these experiments were produced by the injection of gastrotoxic serum. In a form er communication (1) it was demonstrated that the serum, formed by immunising the rabbit with the gastric cells of the guinea-pig or with those of another rabbit, on injection into the guinea-pig's peritoneum produced general symptoms of intoxication and patches of necrosis in the mucous membrane of the stomach. In two later communications (2) and (3) the reactions of gastrotoxin in vitro and its precise mode of action in corpore were demonstrated.

scholarly journals Particularities of Experimental Models Used to Induce Gastric Ulcer

2019 ◽  
Vol 25 (4) ◽  
pp. 179-184
Author(s):  
Simona Fulga ◽  
Ana-Maria Pelin ◽  
Cristina Mihaela Ghiciuc ◽  
Elena Cătălina Lupușoru
Keyword(s):  
Gastric Ulcer ◽  
Hydrochloric Acid ◽  
Experimental Studies ◽  
Experimental Models ◽  
New Drugs ◽  
Laboratory Animals ◽  
Gastric Ulcers ◽  
Current Therapy ◽  
Surgical Methods

Abstract Introduction: Gastric ulcer is one of the most common gastrointestinal diseases, therefore the constant interest for new treatments is due to adverse effects induced by current therapy. The restricted number of in vivo experimental models is a challenge for researchers. Objectives: Identifying the particularities of different types of experimentally induced gastric ulcer in laboratory animals to facilitate their choise for the study of new antiulcer drugs. Material and method: A search in PubMed and Scopus using keywords ( “experimentally” AND “gastric ulcer” AND “rats/mice”) to include experimental studies with the description of local-induced changes. Review articles and in vitro studies were excluded. Results and discussions: Experimental researches on new drugs for gastric ulcer use chemical or surgical methods to induce gastric lesions in rats. Non-steroidal anti-inflammatory drugs (NSAIDs) and acetic acid models to investigate antisecretory and cytoprotective effects; ethanol models evaluate cytoprotective and/or antioxidant effects; pylorus ligature models to evaluate the effects on the secretion of aggressive gastric factors (hydrochloric acid or pepsin). NSAIDs (indomethacin, acetylsalicylic acid or ibuprofen) inhibit cyclooxygenase activity, resulting from reduced mucus and bicarbonate secretion, decreased mucosal blood flow, alteration of microvascular structures, causing epithelial damage Ethanol enhances the proteolytic and hydrolytic action of hydrochloric acid and pepsin; in addition, stimulates the acid secretion and disruptes vascular endothelium. Pylorus ligature determines the accumulation of gastric acid resulting in gastric ulcers due to the autodigestion of the mucosa. Conclusion: The knowledge of the mechanisms to induce experimental gastric ulcers is essential for choosing the model to evaluate new antiulcer agents.

scholarly journals Anti-Inflammatory Effect of Artemisia argyi on Ethanol-Induced Gastric Ulcer: Analytical, In Vitro and In Vivo Studies for the Identification of Action Mechanism and Active Compounds

Plants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 332
Author(s):  
Myoung-Sook Shin ◽  
Jaemin Lee ◽  
Jin Woo Lee ◽  
Se Hoon Park ◽  
Il Kyun Lee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Ulcer ◽  
Molecular Mechanisms ◽  
In Vivo Studies ◽  
Gastric Ulcers ◽  
Mrna Levels ◽  
Griess Reagent ◽  
Artemisia Argyi ◽  
Anti Inflammatory

Artemisia argyi is widely used as traditional medicine in East Asia. However, its effects against inflammation and gastric ulcers have not been reported yet. We analyzed anti-inflammatory activity and its molecular mechanisms of A. argyi using RAW264.7 cells line, then evaluated the curative efficacy in rats with acute gastric ulcers. Nitric oxide and IL-6 production was measured using Griess reagent and an ELISA kit. Inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and mucin (MUC)1, MUC5AC, and MUC6 mRNA were determined by SYBR Green or Taqman qRT-PCR methods. The phosphorylation of ERK, JNK, p38, and c-Jun protein were detected by western blotting. RW0117 inhibited LPS-induced NO and IL-6 production. The mRNA levels of iNOS and IL-6 were strongly suppressed. The phosphorylation of ERK, JNK, and c-Jun decreased by treatment with RW0117. Oral administration of RW0117 recovered the amount of mucin mRNA and protein level that was decreased due to gastric ulcers by HCl-EtOH. A. argyi exhibited strong anti-inflammatory effects and contributed to the modulation of HCl-EtOH-induced gastric ulcer in rats.

Bacterial colonization and healing of gastric ulcers: the effects of epidermal growth factor

2000 ◽  
Vol 278 (1) ◽  
pp. G105-G112 ◽  
Author(s):  
Susan N. Elliott ◽  
J. L. Wallace ◽  
W. McKnight ◽  
D. G. Gall ◽  
J. A. Hardin ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Bacterial Colonization ◽  
Neutrophil Infiltration ◽  
Gastric Ulcers ◽  
Gastric Ulcer Healing ◽  
Epidermal Growth

.—Experimental gastric ulcers are rapidly colonized by various bacteria, resulting in significantly impaired healing. Epidermal growth factor (EGF) is capable of preventing bacterial colonization of the healthy intestinal mucosa. In this study, we examined the possibility that EGF accelerates gastric ulcer healing by reducing bacterial colonization of the ulcer. Gastric ulcers were induced by serosal application of acetic acid. The effect of daily administration of EGF on ulcer healing and bacterial colonization was assessed and compared with the effect of daily treatment with broad-spectrum antibiotics. EGF administration reduced colonization levels and accelerated ulcer healing as effectively as the antibiotic treatment. EGF was without effect on acid secretion or neutrophil infiltration into the ulcer. Bacterial growth was not inhibited in the presence of EGF in vitro. These results demonstrate that EGF reduces bacterial colonization during an established infection of a compromised mucosal surface. This effect may contribute to the ability of EGF to accelerate gastric ulcer healing. This effect is acid independent and not due to an anti-inflammatory effect or to direct bactericidal actions.

scholarly journals In Vitro Framework to Assess the Anti-Helicobacter pylori Potential of Lactic Acid Bacteria Secretions as Alternatives to Antibiotics

2021 ◽  
Vol 22 (11) ◽  
pp. 5650
Author(s):  
Samantha A. Whiteside ◽  
Mahi M. Mohiuddin ◽  
Sargon Shlimon ◽  
Jaspreet Chahal ◽  
Chad W. MacPherson ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Bioactive Molecules ◽  
Gastric Ulcers ◽  
Gastric Cells ◽  
Pre Treatment ◽  
H Pylori ◽  
Pro Inflammatory Cytokines

Helicobacter pylori is a prevalent bacterium that can cause gastric ulcers and cancers. Lactic acid bacteria (LAB) ameliorate treatment outcomes against H. pylori, suggesting that they could be a source of bioactive molecules usable as alternatives to current antibiotics for which resistance is mounting. We developed an in vitro framework to compare the anti-H. pylori properties of 25 LAB and their secretions against H. pylori. All studies were done at acidic and neutralized pH, with or without urea to mimic various gastric compartments. Eighteen LAB strains secreted molecules that curtailed the growth of H. pylori and the activity was urea-resistant in five LAB. Several LAB supernatants also reduced the urease activity of H. pylori. Pre-treatment of H. pylori with acidic LAB supernatants abrogated its flagella-mediated motility and decreased its ability to elicit pro-inflammatory IL-8 cytokine from human gastric cells, without reverting the H. pylori-induced repression of other pro-inflammatory cytokines. This study identified the LAB that have the most anti-H. pylori effects, decreasing its viability, its production of virulence factors, its motility and/or its ability to elicit pro-inflammatory IL-8 from gastric cells. Once identified, these molecules can be used as alternatives or complements to current antibiotics to fight H. pylori infections.

Über die Wirkung von Heparin, Heparinoiden und Carrageenin auf die Komponenten des Meerschweinchen-Komplements in vitro

1965 ◽  
Vol 20 (6) ◽  
pp. 575-581 ◽  
Author(s):  
K. Lauenstein ◽  
H. G. Siedentopf ◽  
H. Fischer
Keyword(s):  
Guinea Pig ◽  
Complement System ◽  
Mode Of Action ◽  
Preceding Paper ◽  
Inhibitory Effect ◽  
The Complement System ◽  
Pig Serum

The mode of action of six inhibitors of the complement system of guinea pig serum was analysed by use of the method described in the preceding paper.Carrageenin is the most powerful inhibitor followed by polyvinylalcoholsulfate, polyethenesulfate, heparinoid “Bayer”, dextransulfate, and heparin. All six substances are directed against C′ 1 and C′ 2. Heparin and polyethenesulfate also inhibit C′ 3b,β, while an effect of heparinoid “Bayer”, dextransulfate, and polyvinylalcoholsulfate upon C′ 3b,β could not definitely be demonstrated. It is not clear whether these latter substances act upon C′ 3b,β, C′ 3c,d, or upon both components.All substances tested exert the strongest inhibitory effect upon C′ 1 which thus becomes the limiting component in guinea pig complement.

Gastric Fibrinolysis

1975 ◽  
Vol 34 (02) ◽  
pp. 409-418 ◽  
Author(s):  
I. M Nilsson ◽  
S.-E Bergentz ◽  
U Hedner ◽  
K Kullenberg
Keyword(s):  
Gastric Ulcer ◽  
Gastric Juice ◽  
High Activity ◽  
Fibrinolytic Activity ◽  
Duodenal Juice ◽  
Bleeding Tendency ◽  
Local Fibrinolysis ◽  
Heated Plates

SummaryGastric juice from 15 normals, 20 patients with gastric ulcer and 4 patients with erosive haemorrhagic gastroduodenitis was investigated in respect of its activity on unheated and heated fibrin plates and its content of FDP and plasminogen or plasmin with immunochemical methods. Gastric juice from normals showed no activity on unheated and heated fibrin plates, and no FDP or plasminogen could be demonstrated. In the patients with gastric ulcer the gastric juice showed little or no fibrinolytic activity on fibrin plates except in 2, who had regurgitation of duodenal juice and neutral pH of the juice. These patients had equally high activity on heated as on unheated plates and no plasmin could be demonstrated. It was shown that this activity was not due to fibrinolysis, but to non-specific proteolytic activity (probably trypsin). The patients with erosive haemorrhagic gastroduodenitis exhibited quite a different picture. The gastric juice from these patients showed extremely high activity on fibrin plates, the activity was higher on unheated than on heated plates. The activity was inhibited in vitro by addition of EACA and in vivo after administration of AMCA. The occurrence of plasmin could be demonstrated directly immunologically in the gastric juice. By comparison of plasmin and trypsin in various assays it could further be proved that the gastric juice in these cases contained plasminogen activator and plasmin. The patients with erosive haemorrhagic gastroduodenitis showed no increase in fibrinolysis in the blood, but low values for plasminogen and α2M, and the serum contained FDP. These findings in the blood and gastric juice were interpreted as signs of local fibrinolysis in the stomach and duodenum. There is reason to assume that this gastric fibrinolysis contributes substantially to the bleeding tendency. The effect of administration of AMCA on fibrinolytic activity and the haemorrhage lends support to the assumption of such a mechanism.

Inhibition of Human and Animal Platelet Adhesiveness to Glass Bead Columns by Adenosine, Dipyridamole, Chlorpromazine and Acetylsalicylic Acid

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu
Keyword(s):  
Guinea Pig ◽  
Acetylsalicylic Acid ◽  
Guinea Pigs ◽  
Glass Bead ◽  
Animal Species ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adhesiveness

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.

INHIBITION OF LIPOLYTIC ACTIVITY OF SYNTHETIC β1–24 AND β1–39 CORTICOTROPHIN BY ANTI-ACTH ANTISERUM

1966 ◽  
Vol 51 (1) ◽  
pp. 88-94 ◽  
Author(s):  
A. Villanueva ◽  
S. J. H. Ashcroft ◽  
J. P. Felber
Keyword(s):  
Guinea Pig ◽  
Lipolytic Activity ◽  
Peptide Hormones ◽  
Fat Pad ◽  
Double Antibody ◽  
Epididymal Fat ◽  
Antibody Complex ◽  
Radio Immunoassay ◽  
Antigen Antibody

ABSTRACT The synthetic ACTH peptides β1–39 and β1–24 stimulated lipolysis as determined by the rat epididymal fat pad in vitro. The stimulating effect of these peptides was diminished by prior incubation of the peptides with antibodies produced by the guinea-pig against ACTH. The stimulating effect of these hormones was also diminished by the double antibody system used in the radio-immunoassay of ACTH and other peptide hormones, in which incubation with antiserum is followed by precipitation of the antigen-antibody complex by rabbit anti-guinea-pig-γ-globulin.

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