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Biomedical subjects

A Tarnawski

Publications and source records attributed to A Tarnawski.

196 records · Page 11Linked to original sources
PubMedDate not supplied

16,16-dimethyl-PGE2 protection against alpha-naphthylisothiocyanate-induced experimental cholangitis in the rat.

Male rats were treated with subcutaneous vehicle or 16,16-dimethyl-PGE2 (dmPGE2, 100 micrograms per kg), 24, 18 and 0.5 hr prior to and 6, 24 and 30 hr after challenge with oral alpha-naphthylisothiocyanate (ANIT, 30 mg per kg). Forty-eight hours after challenge, rats were sacrificed by decapitation; serum and liver samples were taken for biochemical and histological analysis, respectively. Rats treated with vehicle (2% ethanol in saline) and ANIT exhibited elevations in alkaline phosphatase, SGPT and bilirubin as well as cholangitis and mild parenchymal necrosis. Rats treated with dmPGE2 and ANIT had normal serum biochemical findings, no necrosis and only mild proliferation of bile duct epithelium. Thus, dmPGE2 may be able to protect the rat liver against the deleterious effects of orally administered ANIT.

1-Naphthylisothiocyanate↗
PubMedDate not supplied

Regeneration of gastric mucosa during ulcer healing is triggered by growth factors and signal transduction pathways.

An ulcer is a deep necrotic lesion penetrating through the entire thickness of the gastrointestinal mucosa and muscularis mucosae. Ulcer healing is a complex and tightly regulated process of filling the mucosal defect with proliferating and migrating epithelial and connective tissue cells. This process includes the re-establishment of the continuous surface epithelial layer, glandular epithelial structures, microvessels and connective tissue within the scar. Epithelial cells in the mucosa of the ulcer margin proliferate and migrate onto the granulation tissue to re-epithelialize the ulcer. Growth factors, such as epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), trefoil peptides (TP), platelet derived growth factor (PDGF) and other cytokines produced locally by regenerating cells, control re-epithelialization and the reconstruction of glandular structures. These growth factors, most notably EGF, trigger epithelial cell proliferation via signal transduction pathways involving EGF-R- MAP (Erk1/Erk2) kinases. Granulation tissue, which develops at the ulcer base, consists of fibroblasts, macrophages and proliferating endothelial cells, which form microvessels under the control of angiogenic growth factors. These growth factors [bFGF, vascular endothelial growth factor (VEGF) and angiopoietins] promote angiogenesis--capillary vessel formation--thereby allowing for the reconstruction of microvasculature in the mucosal scar, which is essential for delivery of oxygen and nutrients to the healing site. The primary trigger to activate expression of angiogenic growth factors and their receptors appears to be hypoxia. During ulcer healing expression of growth factor genes is tightly regulated in a temporally and spatially ordered manner.

Animals↗
PubMedDate not supplied

The antacid Talcid adsorbs and neutralizes all proteins secreted by H. pylori including VacA cytotoxin: a new mechanism for its ulcer-healing action?

BACKGROUND AND AIM: Helicobacter pylori culture supernatant containing VacA cytotoxin significantly inhibits gastric cell proliferation and delays healing of experimental gastric ulcers. Since cell proliferation is crucial for ulcer healing, the removal of inhibitory effects of H. pylori secreted cytotoxin would have a beneficial effect on the healing process. In this study, we determined whether the antacid Talcid can adsorb, remove, or neutralize H. pylori derived VacA cytotoxin responsible for the above deleterious actions. METHODS: Supernatants of viable H. pylori isogenic strains producing VacA cytotoxin [VacA(+)] and with disrupted cytotoxin gene not producing cytotoxin [VacA(-)] were incubated with either placebo, Talcid 10 mg/ml, omeprazole 10 mg/ml (positive control) for 1-24 h. Treated supernatants were analyzed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis to evaluate proteins. We also studied the effect of supernatants on epidermal growth factor stimulated Kato III cell proliferation using BrdU labeling. RESULTS: Talcid very effectively removed from the H. pylori culture supernatant the approximately 90 kD VacA(+) cytotoxin at 3 and 24 h (99.5% removal vs. placebo-treated control; p<0.001). It also removed all other proteins, including 66-kD urease and 58-kD heat shock protein, secreted by both VacA(+) and VacA(-) H. pylori strains. Omeprazole was completely ineffective in this regard. Preincubation with Talcid completely abolished the inhibitory effect of VacA(+) H. pylori culture supernatant on epidermal growth factor stimulated Kato III cell proliferation. CONCLUSION: Adsorption and neutralization by Talcid of all H. pylori secreted proteins may explain, at least in part, the ulcer-healing action of this drug.

Aluminum Hydroxide↗
PubMedDate not supplied

Effect of Helicobacter pylori culture supernatant on acute reflux esophagitis in a rat model.

BACKGROUND/AIMS: Prevalence of Helicobacter pylori, especially cagA-positive strains is inversely related to gastroesophageal reflux disease. The aim of this study was to examine whether H. pylori culture supernatants affect acute esophagitis induced by acid or mixed reflux in rats. METHODOLOGY: Three different H. pylori strains were used. Acute esophagitis was induced in 59 male Wistar rats by ligation of both the transitional regions between the forestomach and glandular portion, and the pylorus or the lower part of duodenum. After operation, the rats were either left untreated or treated with intragastric injection of either vehicle or H. pylori culture supernatants and were sacrificed 6 or 24 hours later. Esophagitis index, depth of esophageal lesions, esophageal epithelial degeneration, and infiltration of inflammatory cells were examined. RESULTS: Gross esophageal erosions and ulcers were observed up to mid-esophagus in all animals. H. pylori culture supernatants did not affect esophageal mucosal injury and no histologically significant differences were found among rats. CONCLUSIONS: H. pylori culture supernatants, regardless of cagA gene expression, did not affect acute esophagitis induced by acid or mixed reflux. This finding suggests that no powerful protective factors against reflux-induced mucosal injury were produced by H. pylori.

Acute Disease↗
PubMedDate not supplied

Effect of secretin on antipyrine elimination during extracorporeal perfusion of the isolated guinea pig liver.

The aim of these investigations was to elucidate in which part of the bile system (canaliculi or ductules) antipyrine is secreted actively into bile during extracorporeal perfusion of isolated guinea pig liver. Twelve perfusions were performed including 6 control and 6 with secretin. After 1, 2 and 3 hours from the onset of perfusion the perfusion fluid and bile samples were taken for determination of antipyrine concentration. It was demonstrated that secretin increases the volume of secreted bile, the concentration of antipyrine was decreased and the total amount of antipyrine eliminated with bile remained unchanged. The obtained results refute the hypothesis that antipyrine is secreted into bile in the ductular phase and suggest that this process takes place at the level of biliary canaliculi.

Animals↗
PubMedDate not supplied

Phenazone metabolism during perfusion of isolated guinea pig liver.

After 3 hr of perfusion of isolated guinea pig liver with a medium containing 407 ng/ml of phenazone, the drug concentration in the bile was 1.5 times higher than the initial concentration in the perfusion fluid. This indicates that in addition to phenazone metabolism, liver eliminates the drug by active releasing it to the bile. The active release is responsible for depression of phenazone concentration during the perfusion in approx. 6%. The remaining loss of phenazone is due to its hepatic metabolism.

Animals↗
PubMedDate not supplied

[Cellular and molecular mechanisms of the gastric mucosa: injury of the mucosa and the protective action of antacids].

Gastrointestinal mucosa is exposed to many substances, some made by their own body as HCl, pepsin, etc, others from exogenous origin as NSAIDs, alcohol etc. that injury the mucosa. The body has build protective mechanism against the injury that we describe in the article. We know antacids acts neutralizing the acid a now we know it work as a powerful stimulant of the mucosal protection. This is called cytoprotection and is described in the article.

Antacids↗