sofalcone and Gastritis

"Reflux" gastritis after gastrectomy is associated with various symptoms that are often detrimental to the patients' quality of life. However, prevention of the reflux does not always bring relief from the symptoms of gastritis. Helicobacter pylori (H. pylori) is now considered one of the most important pathogenetic factors in gastritis. The association between H. pylori infection and reflux gastritis after gastrectomy was investigated in the present study.. In total, 115 patients who had undergone gastrectomy were entered in this study. Five biopsy specimens from the gastric remnant were taken during upper GI endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. The histological degree of gastritis was determined according to the score system of Rauws et al.. Forty-six patients (40%) demonstrated H. pylori infection in their stomachs. The prevalence of the infection was significantly higher in patients with conventional gastrectomy than in those with subtotal gastrectomy. The prevalence of H. pylori infection was significantly lower in patients who had undergone gastrectomy more than 4 yr ago. The histological gastritis score in patients with H. pylori infection was significantly higher than in those without H. pylori infection. Furthermore, the eradication of H. pylori in patients with both serious gastritis symptoms and no bile reflux improved the symptoms and significantly decreased the histological gastritis score.. The results suggest that H. pylori is a factor in the pathogenesis of reflux gastritis after gastrectomy.

Topics: Amoxicillin; Anti-Ulcer Agents; Chalcone; Chalcones; Drug Therapy, Combination; Female; Gastric Mucosa; Gastric Stump; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Penicillins; Postgastrectomy Syndromes; Prevalence; Risk Factors

We investigated the therapeutic effects of egualen sodium (KT1-32), a new antiulcer agent, on chronic erosive and atrophic gastritis induced by 5 months' administration of sodium taurocholate (TCA; 5 mM) in rats. The chronic gastritis was manifested by mucosal surface injuries (erosions), reduced mucosal thickness, reduction of the number of parietal cells, infiltration of inflammatory cells, and proliferation of collagenous fiber. Egualen sodium, (10-100 mg/kg, t.i.d.) administered orally to the rats for 2 weeks after the withdrawal of TCA, dose-dependently and significantly decreased the total length of erosions. The indicators of atrophic gastritis, i.e., reduced mucosal thickness and reduction in the number of parietal cells, were improved dose-dependently by the administration of this agent. Egualen sodium also reduced the inflammatory cell infiltration and the proliferation of collagenous fiber in the gastric mucosa in a dose-dependent manner. The reduced staining of neutral gastric mucus was improved by a high dose (100 mg/kg) of egualen sodium. The therapeutic effects of egualen sodium on experimental gastritis were superior to those of sofalcone and sodium guaiazulene 3-sulfonate. These results suggest that egualen sodium may be a promising agent for the treatment of erosive and atrophic gastritis.

Topics: Administration, Oral; Animals; Anti-Infective Agents; Anti-Ulcer Agents; Azulenes; Cell Count; Cell Division; Chalcone; Chalcones; Chronic Disease; Dose-Response Relationship, Drug; Gastric Mucosa; Gastritis; Male; Mucus; Parietal Cells, Gastric; Rats; Rats, Wistar; Sesquiterpenes; Sesquiterpenes, Guaiane; Taurocholic Acid; Treatment Outcome

The effect of sofalcone on the glandular structure and cell proliferation in the gastric mucosa of rats with gastritis induced by the administration of sodium taurocholate (TCA) for 6 months was examined by histoquantitative analysis and [3H]thymidine autoradiography. Morphometric observation revealed that, with TCA treatment, mucosal thickness, parietal cell mass, and the ratios of the length of the glandular portion/total length of the gastric gland were decreased in both the fundic and pyloric glands. Inflammatory cell infiltration and collagenous fiber proliferation were present in the gastric mucosa following TCA and indicated the presence of atrophic gastritis. These atrophic changes and inflammatory cell infiltration were reversed by a 3 week administration of sofalcone. Cellular proliferative activity assessed by the labeling indices of the gastric mucosa increased in TCA-induced gastritis in rats. The administration of sofalcone to rats with TCA-induced gastritis significantly increased labeling indices, particularly in the pyloric glands. From these results, it appears that sofalcone stimulates the compensatory increase in proliferative activity of generative cells, which then may become available to heal the gastritis.

Topics: Animals; Anti-Ulcer Agents; Autoradiography; Cell Division; Chalcone; Chalcones; Gastric Mucosa; Gastritis; Male; Rats; Rats, Inbred Strains; Taurocholic Acid; Wound Healing

Changes in gastric mucous glycoprotein (GP) and effects of the anti-ulcer agent, sofalcone, on experimental gastritis induced by 3 or 6 months administration of sodium taurocholate (TCA) were investigated. Macromolecular mucous GP determined as the hexose content, which was fractionated by gel filtration, was decreased with the development of gastritis. This was also demonstrated by the histochemical observations. Soluble mucus, which is easily released into the incubation medium, was significantly decreased, and the insoluble mucus remaining in the gastric mucosa was not changed in 3-month-old gastritis. On the other hand, insoluble mucus was significantly decreased in 6-month-old gastritis. Synthetic activity of mucous GP, which was determined by incorporation of [3H]-glucosamine and [35S]-sulfate, was not changed in 3-month-old gastritis, but, it was markedly decreased in 6-month-old gastritis. The decrease in the content and the synthetic activity of macromolecular mucous GP in 6-month-old gastritis were significantly normalized by 3 weeks administration of sofalcone. The histochemical study also supported the therapeutic effect of sofalcone. These findings suggest that the therapeutic effect of sofalcone on experimental gastritis is closely associated with increased mucus synthesis.

Topics: Animals; Anti-Ulcer Agents; Chalcone; Chalcones; Gastric Mucosa; Gastritis; Gastritis, Atrophic; Glycoproteins; Hexoses; Histocytochemistry; Male; Propiophenones; Rats; Rats, Inbred Strains; Taurocholic Acid; Time Factors

Effects of sofalcone on the morphometrical glandular structure and the generative cell proliferation in the gastric mucosa of gastritis, induced in rats by the treatment of sodium taurocholate (TCA) for 3 and 6 months, were examined by means of 3H-thymidine autoradiography. Morphometrical observation revealed that the ratios of the length of the glandular portion/the total length of the gastric gland were generally decreased in both fundic and pyloric glands with TCA treatments, which may indicate mucosal atrophy. These atrophic changes were improved to the normal levels by the administration of sofalcone for 3 weeks after the treatment of TCA. On the other hand, cell proliferative activity, indicated by the labeling indexes in the generative cell zone of gastric mucosa, was increased in TCA induced gastritis rat, which seems to be the response to replace the increased cell loss. The administration of sofalcone to the gastritis rats further increased the labeling indexes, especially in pyloric gland with statistical significance in both TCA treated rats for 3 and 6 months. From these results, it is suggested that sofalcone stimulates the compensatory increase of proliferative activity of generative cells, which would be available to repair the gastric mucosa with gastritis.

Topics: Animals; Anti-Ulcer Agents; Autoradiography; Cell Division; Chalcone; Chalcones; Gastric Mucosa; Gastritis; Male; Propiophenones; Rats; Rats, Inbred Strains; Taurocholic Acid

A study was made on the therapeutic effects of sofalcone (SU-88), an antiulcer agent, on erosive and atrophic gastritis induced experimentally by 6-month administration of 5 mmol/l of sodium taurocholate (TCA) in rats. A standard meal including sofalcone of 0.25% and 1.0% shortened the total length of erosions, normalized the mucosal thickness, and reduced collagenous fibers in the gastric mucosa in one month. The doses administered were 116.3 mg and 486.1 mg/kg/week for one month. Sofalcone, thus, had a good therapeutic effect on experimental erosive and atrophic gastritis in rats.

Topics: Animals; Anti-Ulcer Agents; Body Weight; Cell Division; Chalcone; Chalcones; Gastric Mucosa; Gastritis; Male; Propiophenones; Rats; Rats, Inbred Strains

The effects of sodium taurocholate (TCA) and sofalcone on prostaglandin (PG) metabolism in rat gastric mucosa were examined. TCA administration for 3 months increased the activity of the PG-metabolizing enzyme, 15-hydroxy-PG-dehydrogenase (15-OH-PG-DH) and decreased the PGE2 content in the rat gastric mucosa. The administration of sofalcone for 3 weeks prevented the increase in the 15-OH-PG-DH activity and prevented the decrease in the PGE2 content reduced by TCA administration. The activation and inhibition of 15-OH-PG-DH activity by the administration of TCA and sofalcone were both uncompetitive and non competitive against the substrates PGE1 and NAD, respectively. These results suggest that the decrease in PGE2 content by the activation of 15-OH-PG-DH activity is involved in the development of TCA induced gastritis and the effect of sofalcone which prevented the decrease of mucosal PGE2 by inhibiting 15-OH-PG-DH plays an important role in the healing of gastritis.

Topics: Animals; Anti-Ulcer Agents; Chalcone; Chalcones; Dinoprostone; Gastric Mucosa; Gastritis; Hydroxyprostaglandin Dehydrogenases; Kinetics; Male; Propiophenones; Prostaglandins E; Rats; Rats, Inbred Strains; Taurocholic Acid

Sofalcone prevented the formation of lesions by 50% ethanol and aspirin dose dependently, prevented the decrease in the gastric mucosal macromolecular glycoprotein content caused by these treatments, and prevented the decrease in the incorporation of 3H-glucosamine caused by ethanol and aspirin into the macromolecular glycoprotein. 35S-Sulfate incorporation, which was slightly decreased, by the administration of ethanol and aspirin, was significantly increased, and the specific activity of sulfated macromolecular glycoprotein synthesis which was not changed by ethanol or aspirin was increased by the administration of sofalcone prior to these treatments. These results suggest that the maintenance of the mucosal macromolecular glycoprotein content is involved in the protective effects of sofalcone against the formation of acute gastric lesions induced by ethanol and aspirin.

Topics: Animals; Aspirin; Chalcone; Chalcones; Ethanol; Gastric Mucosa; Gastritis; Glucosamine; Glycoproteins; Male; Propiophenones; Rats; Sulfates; Tranexamic Acid