peptones and Disease-Models--Animal

Helicobacter pylori (H. pylori) is an obligate microaerobion and does not survive in low oxygen. Sodium sulfite (SS) reacts and consume oxygen in solutions. The present study aimed to investigate the effects of SS on H. pylori. The effects of SS on oxygen concentrations in solutions and on H. pylori in vivo and in vitro were examined, and the mechanisms involved were explored. The results showed that SS decreased the oxygen concentration in water and artificial gastric juice. In Columbia blood agar and special peptone broth, SS concentration-dependently inhibited the proliferation of H. pylori ATCC43504 and Sydney strain-1 in Columbia blood agar or special peptone broth, and dose-dependently decreased the number of H. pylori in Mongolian gerbils and Kunming mouse infection models. The H. pylori was relapsed in 2 weeks withdrawal and the recurrence in the SS group was lower than that in the positive triple drug group. These effects were superior to positive triple drugs. After SS treatments, the cell membrane and cytoplasm structure of H. pylori were disrupted. SS-induced oxygen-free environment initially blocked aerobic respiration, triggered oxidative stress, disturbed energy production. In conclusion, SS consumes oxygen and creates an oxygen-free environment in which H. pylori does not survive. The present study provides a new strategy and perspective for the clinical treatment of H. pylori infectious disease.

Topics: Agar; Animals; Disease Models, Animal; Gastric Mucosa; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Mice; Peptones

Fucosylated chondroitin sulfate

Topics: Animals; Anti-Inflammatory Agents; Cartilage; Chondroitin Sulfates; Circular Dichroism; Cucumaria; Disease Models, Animal; Female; Humans; Magnetic Resonance Spectroscopy; Molecular Structure; Peptones; Peritonitis; Rats; Rats, Wistar; Salmo salar; Structure-Activity Relationship; Treatment Outcome

Neuropeptide Y (NPY), a centrally located neurotransmitter, is known to increase appetite in fasted and satiated animals. In addition to evaluating NPY's effect on eating behavior, this study was intended to determine whether intracerebroventricular (ICV) NPY would have an effect on canine gastric and pancreatic secretion.. Four dogs were prepared with cerebroventricular guides and gastric and pancreatic fistulas. ICV and intravenous NPY was administered during intragastric titration of a glucose and peptone meal. During this study, gastric and pancreatic secretion was measured, as well as insulin levels and pancreatic polypeptide (PP). An additional set of four dogs were prepared with esophageal fistulas and cerebroventricular guides, and the effect of ICV NPY on sham feeding was studied.. ICV NPY significantly increased sham feeding, meal-stimulated gastric and pancreatic secretion, basal gastric acid, pancreatic bicarbonate, insulin levels, and PP. Vagotomy blocked the effect of ICV NPY on gastric acid secretion in a urethane-anesthetized rat model with acute gastric fistula.. ICV NPY increased sham feeding, gastric and pancreatic secretion, insulin levels, and PP in the dogs. NPY's effect on gastric secretion was blocked by vagotomy in a rat model. NPY should be considered a candidate mediator of cephalic phase secretion.

Topics: Analysis of Variance; Animals; Bicarbonates; Disease Models, Animal; Dogs; Eating; Female; Gastric Acid; Gastric Acidity Determination; Gastric Fistula; Gastric Mucosa; Glucose; Injections, Intravenous; Injections, Intraventricular; Insulin; Insulin Secretion; Male; Neuropeptide Y; Pancreas; Pancreatic Polypeptide; Peptones; Rats; Rats, Sprague-Dawley; Vagus Nerve

The rat subcutaneous air pouch model was adapted to examine the in vivo degradation of implanted rabbit articular cartilage, both with and without induced air pouch inflammation, over a 7-day period. The effects of 3 drugs, glycosaminoglycan polysulfate (Arteparon), pentosan polysulfate (SP-54), and zinc-chelated pentosan polysulfate (DH-40J), on inflammation-induced cartilage degradation were also examined. Implanted articular cartilage from noninflamed air pouches showed a reduction in total proteoglycan (PG) content (as hexuronic acid), but not in PG extractability or aggregation, compared with cartilage maintained in tissue culture. The injection of peptone into the air pouch as an inflammogen caused an influx of leukocytes and plasma exudate and a reduction in implanted articular cartilage PG content, extractability, and aggregation, which was significantly greater than that which occurred in noninflamed air pouches. In vitro experiments demonstrated that peptone did not have a direct effect on cartilage PG degradation. Daily injection of Arteparon, SP-54, or DH-40J (10 mg/kg) into peptone-inflamed air pouches significantly increased the PG content, extractability, and aggregation in implanted articular cartilage, compared with that in cartilage from non-drug-treated control animals. The infiltration of leukocytes into the peptone-inflamed air pouches was significantly reduced by daily administration of Arteparon, 10 mg/kg. At an equivalent dose, DH-40J increased leukocyte numbers in the pouch fluid, whereas SP-54 had no significant effect on leukocyte accumulation.

Topics: Animals; Cartilage, Articular; Disease Models, Animal; Female; Glycosaminoglycans; In Vitro Techniques; Inflammation; Male; Pentosan Sulfuric Polyester; Peptones; Polysaccharides; Proteoglycans; Rabbits; Rats; Rats, Inbred Strains

The method of intrapulmonary infection of guinea pigs was suggested for the assessment of the virulent properties of cholera vibrios. Addition into the diluent of 10% peptone, 10% gelatine and 0.05% agar-agar led to the reduction of LD50 by over 1000 times. A specific infectious process coursing in an acute generalized form with bacteriemia and affection of the small intestine developed in the infected animals. The majority of the animals perished in 1 to 2 days.

Topics: Agar; Animals; Cholera; Disease Models, Animal; Gelatin; Guinea Pigs; Lethal Dose 50; Peptones; Vibrio cholerae; Virulence