sofalcone and Stomach-Ulcer

sofalcone has been researched along with Stomach-Ulcer* in 20 studies

Reviews

1 review(s) available for sofalcone and Stomach-Ulcer

ArticleYear
The possible role of vascular endothelial growth factor (VEGF) in gastric ulcer healing: effect of sofalcone on VEGF release in vitro.
    Journal of clinical gastroenterology, 1998, Volume: 27 Suppl 1

    Angiogenesis plays an important role in gastric ulcer repair. Several growth factors are involved in angiogenesis and, of these, vascular endothelial growth factor (VEGF) has received considerable attention because it is the only factor that acts specifically on endothelial cells and, unlike other angiogenic growth factors, has the hydrophobic signal peptide required for extracellular transport according to classical secretory pathways. We have lately demonstrated the role of VEGF in gastric ulcer repair. Previous reports confirmed that sofalcone has remarkable effects on gastric ulcer healing, which may be mediated by its stimulatory effect on prostaglandin (PG) release in gastric cells. Our data indicate that PGs stimulate VEGF expression in gastric fibroblasts. In this report we hypothesize that the clinical effect of sofalcone is mediated by VEGF expression and we demonstrate that sofalcone stimulates VEGF release by gastric fibroblasts in primary culture.

    Topics: Anti-Ulcer Agents; Chalcone; Chalcones; Endothelial Growth Factors; Humans; Lymphokines; Neovascularization, Physiologic; Regeneration; Stomach Ulcer; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors

1998

Trials

1 trial(s) available for sofalcone and Stomach-Ulcer

ArticleYear
Sofalcone, a gastroprotective drug, promotes gastric ulcer healing following eradication therapy for Helicobacter pylori: a randomized controlled comparative trial with cimetidine, an H2-receptor antagonist.
    Journal of gastroenterology and hepatology, 2010, Volume: 25 Suppl 1

    According to reports in Japanese patients, 1 week of Helicobacter pylori eradication therapy alone is not adequate for healing of gastric ulcers; 7-8 weeks of anti-ulcer therapy are subsequently required. We compared a gastroprotective drug, sofalcone, and an H(2)-receptor antagonist, cimetidine, in terms of promoting ulcer healing after 7 weeks of administration following 1 week of eradication therapy.. Eradication therapy was administered to 64 patients with H. pylori-positive active gastric ulcer at least 10 mm in diameter, after which 32 patients each received 7 weeks of ulcer treatment with sofalcone (300 mg/day) or cimetidine (800 mg/day).. The H. pylori eradication rate was 81.3% (intention-to-treat: ITT) and 81.3% (per protocol: PP) in the sofalcone group, and 62.5% (ITT) and 64.5% (PP) in the cimetidine group. The ulcer healing rate after 8 weeks was 71.9% (ITT) and 71.9% (PP) in the sofalcone group, and 71.9% (ITT) and 71.0% (PP) in the cimetidine group. The rate of a flat pattern of scarred mucosa was 43.5% (ITT) and 43.5% (PP) in the sofalcone group, and 47.8% (ITT) and 50.0% (PP) in the cimetidine group. No significant differences were seen between the two groups in terms of H. pylori eradication rate, ulcer healing rate and flat pattern rate.. Sofalcone promoted gastric ulcer healing during 7 weeks of treatment following 1 week of eradication therapy, and the healing rate was equivalent to that of cimetidine. Symptom disappearance rates were significantly better in the sofalcone group than in the cimetidine group. This may be a useful way of using a gastroprotective drug in the H. pylori era.

    Topics: Adult; Aged; Anti-Bacterial Agents; Anti-Ulcer Agents; Chalcones; Chi-Square Distribution; Cimetidine; Endoscopy, Digestive System; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Japan; Male; Middle Aged; Stomach Ulcer; Time Factors; Treatment Outcome; Wound Healing

2010

Other Studies

18 other study(ies) available for sofalcone and Stomach-Ulcer

ArticleYear
Gastroprotective effects of flavonoids in plant extracts.
    Journal of physiology and pharmacology : an official journal of the Polish Physiological Society, 2005, Volume: 56 Suppl 1

    The purpose of this paper is to overview the relations between plant-originated substances and their bioactivity measured in terms of antioxidant, cytoprotective and antiulcer activities. In addition, we assessed whether these compounds are capable of affecting the gastric mucosal lesions induced by absolute ethanol applied intragastrically (i.g.). The following plant-originated flavonoid substances were considered; Solon (Sophoradin extract), Amaranth seed extract, grapefruit-seed extract (GSE) and capsaicin (extract of chilly pepper). The area of gastric mucosa lesions and gastric blood flow were measured in rats with ethanol-induced lesions without (control) and with one of the tested substances without and with capsaicin denervation of afferent nerves or administration of L-nitro-arginine (L-NNA), an inhibitor of nitric oxide synthase (NOS). Male Wistar rats, weighing 180-220 g fasted for 24 h before the study where used 100% ethanol was applied i.g. to induce gastric lesions, whose area was determined by planimetry. Gastric blood flow was assessed using electrolytic regional blood flowmeter. All tested plant-originated substances afforded gastroprotection against ethanol-induced damage and this was accompanied by increase in gastric microcirculation, both changes being reversed by pretreatment with neurotoxic dose of capsaicin or by pretreatment with L-NNA. We conclude that plant-originated flavonoid substances are highly gastroprotective probably due to enhancement of the expression of constitutive NOS and release of NO and neuropeptides such as calcitonin gene related peptide (CGRP) released from sensory afferent nerves increasing gastric microcirculation.

    Topics: Animals; Anti-Inflammatory Agents; Anti-Ulcer Agents; Chalcones; Flavonoids; Gastric Mucosa; Male; Plant Extracts; Rats; Rats, Wistar; Stomach Ulcer

2005
Autonomic nervous regeneration in acetic acid-induced ulcer from the viewpoint of synapse formation--effect of basic fibroblast growth factor and sofalcone in the rat.
    Alimentary pharmacology & therapeutics, 2000, Volume: 14 Suppl 1

    Monoclonal antibodies against GAP43 and synaptophysin, markers of regenerated nerves, have recently become available.. To investigate the regeneration of the autonomic nerves after acetic acid treatment, as well as the effect of recombinant basic fibroblast growth factor (bFGF-CS23) and sofalcone on reinnervation.. Ulcers were induced by the direct application of 100% acetic acid to the serosal surface of the rat fundic stomach. Some rats were treated with bFGF-CS23 or sofalcone every 12 h after the acetic acid treatment. The immunohistochemical location of GAP43 and synaptophysin was observed by confocal laser microscopy, and the uptake sites of 14C-sofalcone were observed by autoradiography.. Both GAP43 and synaptophysin immunoreactivities surrounding microvessels were weak in the control group, whereas in the acetic acid-treated group, these immunoreactivities were increased. Treatment with bFGF-CS23 and sofalcone increased these immunoreactivities. The binding sites of sofalcone coincided with the location of regenerated nerves and surface mucous cells. The progenitors of the autonomic nerves were more abundant than expected.. Both bFGF and sofalcone seem to stimulate nerve regeneration.

    Topics: Acetic Acid; Animals; Anti-Ulcer Agents; Autonomic Nervous System; Autoradiography; Binding Sites; Carbon Radioisotopes; Chalcone; Chalcones; Fibroblast Growth Factor 2; Immunohistochemistry; Male; Nerve Regeneration; Rats; Rats, Wistar; Stomach Ulcer; Synaptophysin

2000
The effect of sofalcone on indomethacin-induced gastric ulcers in a Helicobacter pylori-infected gnotobiotic murine model.
    Alimentary pharmacology & therapeutics, 2000, Volume: 14 Suppl 1

    Sofalcone has been reported to exert anti-ulcer and gastroprotective actions, but its exact mechanism of action remains unknown. In our laboratory, we found that indomethacin-induced gastric ulcers become worse when associated with Helicobacter pylori infection.. We employed the H. pylori-infected gnotobiotic murine model to examine the effect of sofalcone on indomethacin-induced gastric ulcers in the presence of H. pylori infection. In vitro experiments were also done to evaluate the effects of sofalcone on H. pylori growth, adherence of H. pylori to the MKN45 cells (a human gastric epithelial cell line), and these cells' IL-8 production in the presence of H. pylori.. We found that sofalcone produced a significant improvement in ulcer size as well as a substantial reduction in the number of H. pylori colonies in H. pylori-infected gnotobiotic mice. In vitro sofalcone has a significant bacteriocidal effect against H. pylori and can also significantly prevent adherence of this bacterium to MKN45 cells, thus remarkably reducing IL-8 production of these cells in response to stimulation by H. pylori.. Our results suggest that sofalcone can improve ulcer healing by the mechanisms mentioned above.

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Cell Adhesion; Chalcone; Chalcones; Disease Models, Animal; Helicobacter Infections; Helicobacter pylori; Humans; Indomethacin; Interleukin-8; Mice; Mice, Inbred BALB C; Stomach Ulcer

2000
A novel in vitro effect of the mucosal protective agent sofalcone--inhibition of chemotactic motility in Helicobacter pylori.
    Alimentary pharmacology & therapeutics, 2000, Volume: 14 Suppl 1

    Motility of Helicobacter pylori is essential for colonization. H. pylori has been shown to exhibit chemotactic activity toward urea and sodium and bicarbonate ions, which are secreted from the gastric epithelia. The importance of urease activity for chemotactic motility of H. pylori in a viscous environment has also been shown. Consequently, application of drugs inhibiting chemotactic motility has been proposed as a strategy for H. pylori eradication. This inhibitory effect can be evaluated through assay of chemotaxis and swarming.. H. pylori CPY3401 and ATCC43504 were grown on brucella agar plates/broth supplemented with 3% horse serum under microaerobic conditions (N2, 85%; O2, 5%; CO2, 10%). For motility assay, H. pylori cells grown on brucella-serum agar were stabbed into motility agar containing 0.35% refined agar in brucella-serum broth and the swarming zone was measured. For the chemotaxis assay, cells were suspended in 10 mM potassium phosphate buffer, pH 7.0, with 3% polyvinyl-pyrrolidone and assayed as described previously. Bacterial swimming in the fluid environment was observed under dark-field microscopy.. Numbers of bacteria attracted toward 1 microM flurofamide were reduced with increasing concentrations of sofalcone (0.2-222 microM). In addition, the size of the swarming zone was reduced in motility agar containing 22 and 222 microM sofalcone. On the other hand, 22 microM sofalcone did not inhibit bacterial growth on day 3. Bacterial swimming speed in brucella broth was slower in the presence of 22 and 222 microM sofalcone than in its absence.. Sofalcone was found to inhibit chemotactic motility of H. pylori. This drug may be useful for inhibiting the bacterium's ability to colonize the human stomach.

    Topics: Anti-Ulcer Agents; Cell Culture Techniques; Chalcone; Chalcones; Chemotaxis; Dose-Response Relationship, Drug; Helicobacter pylori; Humans; Stomach Ulcer; Urease

2000
Effect of combined administration of lansoprazole and sofalcone on microvascular and connective tissue regeneration after ethanol-induced gastric mucosal damage.
    Journal of clinical gastroenterology, 1998, Volume: 27 Suppl 1

    We undertook the present study to clarify the alteration of localization of basic fibroblast growth factor (bFGF), endothelial cells, and myofibroblasts in the healing of ethanol-induced gastric mucosal damage by the combined administration of lansoprazole and sofalcone. Wistar strain male rats were used. Ethanol 50% was given through orogastric intubation. Thirty minutes later, an aqueous solution of lansoprazole, sofalcone, a combination of lansoprazole and sofalcone, or physiologic saline was given orally. The stomach was removed and the localization of bFGF, myofibroblast, and endothelial cells was examined using monoclonal antibodies. Some rats were pretreated with indomethacin to rule out the effect of endogenous prostaglandin. The combined administration of lansoprazole and sofalcone brought about increased concentrations and immunoreactive areas of bFGF and a greater number of endothelial cells, compared with the ethanol-alone treatment. The number of myofibroblasts increased more significantly in the group treated with a combination of agents than in that treated with ethanol alone, ethanol plus sofalcone, or ethanol plus lansoprazole. Indomethacin pretreatment partly abolished the effects of single and combined administration of these agents. In conclusion, the mixed administration of lansoprazole and sofalcone accelerated the microvascular and connective tissue regeneration during the healing of ethanol-induced gastric mucosal damage.

    Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Animals; Anti-Ulcer Agents; CD36 Antigens; Chalcone; Chalcones; Connective Tissue; Drug Therapy, Combination; Endothelium, Vascular; Ethanol; Fibroblast Growth Factor 2; Fibroblasts; Gastric Mucosa; Immunohistochemistry; Irritants; Lansoprazole; Male; Microcirculation; Omeprazole; Rats; Rats, Wistar; Regeneration; Stomach Ulcer

1998
Gastric urease activity is inversely associated with the success of treatment for Helicobacter pylori: effect of sofalcone.
    Journal of clinical gastroenterology, 1998, Volume: 27 Suppl 1

    Eradication therapy for Helicobacter pylori (H. pylori) has been established. However, the physiological factors influencing the success of treatment remain unclear. The aim of this study was to analyze these factors and to evaluate the efficacy of sofalcone on H. pylori eradication therapy. Forty-four H. pylori-infected and peptic ulcer patients were enrolled in this study. Twenty-seven patients were treated with lansoprazole (LPZ, 30 mg o.d. for 1-8 weeks) and amoxicillin (AMPC, 500 mg q.i.d, 1-2 weeks), followed by 8 weeks of treatment with famotidine (FAM, 20 mg o.d.). Moreover, sofalcone (SOF, 100 mg t.i.d) was administered to 17 patients throughout the therapeutic period. Endoscopic and serologic evaluations and the urea breath test (UBT) were performed before therapy. At the endoscopic examination, mucosal samples were biopsied and then tissue myeloperoxidase (MPO) content, an index of neutrophil infiltration was measured. Cure of H. pylori infection was determined 8 weeks after the cessation of LPZ. This eradication regimen afforded an overall cure rate of 63.0% (17/27) without SOF and 76.5% (13/17) with SOF. In the control group, treatment success was inversely associated with pre-UBT value (gastric urease activity), whereas this association was not observed in the SOF group. Furthermore, in the patients exhibiting a high preUBT value (>40%), a twofold higher eradication rate was obtained by the administration of SOF. In patients who were successfully eradicated, mucosal MPO level was slightly higher than those of unsuccessful cases, whereas there was no significant association with serum pepsinogen (PG I, PG II) concentration and its ratio (PG I/PG II). These results suggest that a low UBT value is a factor predicting treatment success. SOF administration may improve the eradication rate, especially in the high-UBT subgroup.

    Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Amoxicillin; Anti-Ulcer Agents; Breath Tests; Carbon Isotopes; Chalcone; Chalcones; Drug Therapy, Combination; Duodenal Ulcer; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Lansoprazole; Male; Middle Aged; Omeprazole; Penicillins; Proton Pump Inhibitors; Stomach Ulcer; Treatment Outcome; Urea; Urease

1998
Alteration of basic fibroblast growth factor concentration and immunoreactivity in healing of ethanol-induced gastric mucosal damage: effect of sofalcone.
    Journal of clinical gastroenterology, 1997, Volume: 25 Suppl 1

    To clarify the interaction of endothelial cells, myofibroblasts, and basic fibroblast growth factor (bFGF) in healing of gastric mucosal damage, histochemical and biochemical observations were undertaken. In addition, the effect of sofalcone on ulcer healing and especially on angiogenesis was studied. Male Wistar rats were used. Ethanol (50%) was administered through an orogastric tube. Thirty minutes after ethanol administration, an aqueous solution of sofalcone (100 mg/100 g b.w.) or the same amount of physiologic saline was administered in the same way. At 1, 3, and 12 h after sofalcone treatment, the localization of endothelial cells and myofibroblasts was studied. The bFGF concentration was decreased at 3 and 12 h in rats treated with ethanol alone, but addition of sofalcone did not alter the content of bFGF 3.5 and 12.5 h after sofalcone administration. Sofalcone had a strong influence on healing of ethanol-induced gastric mucosal damage, possibly through an indomethacin-sensitive, prostanoid-related increase in bFGF concentration.

    Topics: Animals; Anti-Ulcer Agents; Chalcone; Chalcones; Ethanol; Fibroblast Growth Factor 2; Gastric Mucosa; Male; Rats; Rats, Wistar; Stomach Ulcer

1997
Effect of sofalcone on the expression of hepatocyte growth factor (HGF) and a brief review of HGF in the stomach.
    Journal of clinical gastroenterology, 1997, Volume: 25 Suppl 1

    Previous studies of hepatocyte growth factor (HGF) in the stomach are briefly reviewed. Exogenous HGF has a strong effect on proliferation and migration of gastric epithelial cells. These effects of HGF are mediated by the specific receptor c-MET. Our previous immunohistochemical study revealed that the main source of endogenous HGF in human gastric ulcer is gastric fibroblasts. These findings suggest that HGF may play an important role in the repair of gastric ulcers through a paracrine mechanism. Therefore, regulation of HGF expression by gastric fibroblasts may be important. We have demonstrated that prostaglandins (PGs) E1 and E2 strongly stimulate HGF expression by gastric fibroblasts, indicating that the clinical efficacy of PGs is mediated by HGF, PGE1 actually facilitates restitution in an in vitro gastric mucosal model consisting of gastric epithelial cells and fibroblasts, which was completely inhibited by anti-HGF antibody. In this study we investigated the effect of an anti-ulcer drug, sofalcone, on PGE2 release and HGF expression by human gastric fibroblasts in primary culture. Sofalcone induced PGE2 release by human gastric fibroblasts in a dose-dependent manner. It also stimulated HGF expression by gastric fibroblasts, indicating that PGs induced by sofalcone increased HGF expression. These findings suggest that clinical efficacy of PGs and sofalcone might be mediated, at least in part, by HGF.

    Topics: Anti-Ulcer Agents; Cell Division; Cells, Cultured; Chalcone; Chalcones; Dinoprostone; Fibroblasts; Gastric Mucosa; Hepatocyte Growth Factor; Humans; Polymerase Chain Reaction; Proto-Oncogene Proteins c-met; RNA, Messenger; Stomach Ulcer

1997
Effect of 10% ethanol and sofalcone on prostaglandin E2 content, mucus gel thickness, and experimental ulcers in the stomach of developing rats.
    Digestion, 1996, Volume: 57, Issue:1

    We studied the effects of a mild irritant, 10% ethanol, and sofalcone on the gastric mucosal defense mechanisms in newborn rats, comparing the effects to those seen in adult rats. The results indicated (1) that both mucosal prostaglandin E2 (PGE2) content and mucus gel layer thickness increased with age, (2) that sofalcone, but not 10% ethanol, increased mucosal PGE2 content and mucus gel thickness in 1- and 8-week-old rats, (3) that both sofalcone and 10% ethanol decreased mucosal damage induced by 50 or 75% ethanol in both age groups, and (4) that 10% ethanol, but not sofalcone, decreased ethanol-induced mucosal damage in rats pretreated with indomethacin. We concluded that 10% ethanol and sofalcone increase gastric mucosal defence mechanisms in newborn rats as in older rats.

    Topics: Aging; Animals; Animals, Newborn; Anti-Ulcer Agents; Chalcone; Chalcones; Dinoprostone; Dose-Response Relationship, Drug; Ethanol; Female; Gastric Mucosa; Indomethacin; Male; Mucus; Rats; Rats, Wistar; Stomach Ulcer

1996
[Effects of the anti-ulcer agents on the amine contents and regulating enzyme activity of gastric mucosa during the healing process of acetic acid induced gastric ulcer in rats].
    Nihon yakurigaku zasshi. Folia pharmacologica Japonica, 1990, Volume: 95, Issue:1

    In order to elucidate the action of an H2 blocker (cimetidine) and gastric mucosal protection agents (sucralfate and sofalcone) on the relapse and recurrence of gastric ulcer, the effects of cimetidine, sucralfate and sofalcone on the contents of histamine and serotonin and histidine decarboxylase (HDC) activity in the gastric mucosa were examined in the ulcer region and the intact region at the 10th day after the operation to produce acetic acid-induced gastric ulcer in rats. The following results were obtained: 1) HDC activity in the gastric mucosa of rats treated with cimetidine (100 mg/kg twice daily) tended to increase in the intact region, and it was significantly increased in the ulcer region. 2) Increased HDC activity due to cimetidine treatment was observed at the 10th day after interruption of cimetidine administration. 3) The HDC activity in the gastric mucosa was not changed by the treatment with sucralfate (500 mg/kg/day) and sofalcone (200 mg/kg/day). The results suggest that the increased HDC activity in the gastric mucosa might participate in the relapse and recurrence of gastric ulcer after discontinuation of cimetidine administration.

    Topics: Acetates; Animals; Anti-Ulcer Agents; Biogenic Amines; Carboxy-Lyases; Chalcone; Chalcones; Cimetidine; Gastric Mucosa; Histamine H2 Antagonists; Histidine Decarboxylase; Male; Rats; Rats, Inbred Strains; Stomach Ulcer; Sucralfate; Wound Healing

1990
Effects of KB-5492, 1-(3,4,5-trimethoxybenzyl)-4-((4-methoxyphenyl)oxycarbonylmethyl) p iperazine monofumarate monohydrate, on gastric lesions and gastric secretion in rats.
    Japanese journal of pharmacology, 1990, Volume: 53, Issue:2

    Effects of a newly synthesized compound, KB-5492, on gastric lesions and gastric secretion were studied in rats. Oral KB-5492 inhibited the lesions induced by HCl.ethanol, HCl.aspirin, water-immersion stress, indomethacin, histamine and prednisolone at 30-300 mg/kg. The ED50 values varied from about 35 to 98 mg/kg. KB-5492 had no effect on gastric acid secretion even at 300 mg/kg. KB-5492 appeared to have a much more potent protective effect than a known anti-ulcer drug, sofalcone, against acute gastric lesions.

    Topics: Animals; Anti-Ulcer Agents; Chalcone; Chalcones; Gastric Mucosa; Immersion; Male; Piperazines; Rats; Rats, Inbred Strains; Stomach Ulcer; Stress, Physiological

1990
Gastroprotective and ulcer healing effects of solon, a synthetic flavonoid derivative of sophoradin.
    Hepato-gastroenterology, 1987, Volume: 34, Issue:4

    Solon, a synthetic isoprenyl flavonoid derived from sophoradin isolated from the root of an ancient Chinese plant, administered orally to rats, prevented, dose-dependently, the formation of acute gastric lesions produced by absolute ethanol given orally. Solon also enhanced the healing of chronic gastric and duodenal ulcerations induced by the serosal application of acetic acid. The gastroprotective action of Solon was probably mediated by increased mucosal content of prostaglandins (PG) due mainly to the inhibition of 15-OH-prostaglandin dehydrogenase. The ulcer-healing action of Solon was probably related to the stimulation of mucus-alkaline secretion, increased mucosal blood flow and the formation of a protective barrier on the ulcer base.

    Topics: Acetates; Acetic Acid; Animals; Anti-Ulcer Agents; Bicarbonates; Chalcone; Chalcones; Dinoprostone; Ethanol; Gastric Acid; Gastric Mucosa; Male; Pancreas; Peptic Ulcer; Propiophenones; Prostaglandins E; Rats; Rats, Inbred Strains; Regional Blood Flow; Stomach Ulcer

1987
Antiulcer and gastroprotective effects of solon, a synthetic flavonoid derivative of sophoradin. Role of endogenous prostaglandins.
    European journal of pharmacology, 1986, Jun-17, Volume: 125, Issue:2

    Solon is a synthetic isoprenyl flavonoid derived from sophoradin which is isolated from the root of an ancient Chinese plant. Solon was administered orally or intraperitoneally to rats. It inhibited dose dependently gastric ulcers produced by acidified aspirin, water immersion and restraint stress. Solon was also gastroprotective for the stomach as it reduced dose dependently the gastric necrotic lesions induced by absolute ethanol given orally. The degree of gastroprotection decreased with time, the optimal effects occurring 60-90 min after oral administration. Pretreatment with indomethacin partly prevented the gastroprotective effects of Solon. When given alone to fasted rats, Solon increased dose dependently the mucosal content of prostaglandins (PG), suggesting that the protective effects of this drug may be mediated at least in part by endogenous PG.

    Topics: Animals; Anti-Ulcer Agents; Aspirin; Chalcone; Chalcones; Ethanol; Female; Gastric Juice; Indomethacin; Male; Propiophenones; Prostaglandins; Rats; Rats, Inbred Strains; Stomach Ulcer; Stress, Psychological

1986
Cytoprotective effect of sofalcone in the rat gastric mucosa.
    Arzneimittel-Forschung, 1985, Volume: 35, Issue:1

    The effect of 2'-carboxymethoxy-4,4'-bis(3-methyl-2-butenyloxy)-chalcone (sofalcone, Solon) on 0.6N HCl-induced gastric lesions in the rat was studied. Sofalcone administered orally or intraperitoneally prevented the formation of gastric lesions induced by the necrotizing agent dose-dependently. Oral administration of sofalcone inhibited the aggravating effect of indometacin on the lesions induced by 0.6N HCl. Intraperitoneal administration of sofalcone also inhibited the aggravation of the lesions by indometacin treatment when it was given 30 min after the administration of sofalcone. This effect of sofalcone was not observed when indometacin was given 30 min before sofalcone. Simultaneous treatment with sofalcone and cimetidine inhibited the formation of the necrotic lesion synergistically. Carbenoxolone and cetraxate given orally protected the gastric mucosa against 0.6N HCl. Their protective effects were decreased when they were given intraperitoneally. These results suggested that the cytoprotective effect of sofalcone does not depend on the route of administration and that there are some interactions between cimetidine and sofalcone in their synergistic cytoprotective effects.

    Topics: Administration, Oral; Animals; Anti-Ulcer Agents; Carbenoxolone; Chalcone; Chalcones; Cimetidine; Dinoprostone; Gastric Mucosa; Indomethacin; Injections, Intraperitoneal; Male; Propiophenones; Prostaglandins E; Rats; Rats, Inbred Strains; Stomach Ulcer

1985
Effect of 2'-carboxymethoxy-4,4'-bis(3-methyl-2-butenyloxy) chalcone (sofalcone) on chronic gastric ulcers in rats.
    Japanese journal of pharmacology, 1984, Volume: 35, Issue:4

    The anti-ulcer effect of sofalcone, an isoprenyl chalcone derivative, on acetic acid-induced gastric ulcers in rats was studied histologically and histochemically. After administrations of sofalcone at 50 and 200 mg/kg twice daily for 10 days, contraction of the ulcer, mucosal regeneration, accelerated development of the collagen fibers in the granulation tissue at the base of the ulcer, and increase of acid mucopolysaccharides, an alcian blue stain-positive substance covering the regenerated mucosa, were noted. The healing effect of sofalcone was balanced in mucosal regeneration and connective tissue proliferation (formation of the collagen fibers). Sofalcone of 50 mg/kg showed a greater healing effect than gefarnate at the same dose and had a similar healing effect as L-glutamine at 200 mg/kg.

    Topics: Acetates; Acetic Acid; Animals; Anti-Ulcer Agents; Cell Division; Chalcone; Chalcones; Gastric Mucosa; Gefarnate; Glutamine; Male; Propiophenones; Rats; Rats, Inbred Strains; Staining and Labeling; Stomach Ulcer

1984
Cytoprotective effect of SU-88, an anti-ulcer agent, in the rat.
    Japanese journal of pharmacology, 1984, Volume: 35, Issue:1

    The gastric cytoprotective action of SU-88, an anti-ulcer agent, was studied in rats. SU-88 dose-dependently prevented the formation of gastric lesions induced by absolute ethanol as observed by PGE2. The efficacy of SU-88 when given i.p. was more potent than the p.o. administration. Indomethacin (5mg/kg, p.o.) given 30 min prior to SU-88 dosing blocked this protective effect, whereas it was not affected when indomethacin was given 30 min after the SU-88 dosing. Cimetidine, on the other hand, failed to exert a protective effect against the ethanol-induced lesions and caused a significant increase in the lesions induced by 0.6N HCI. Pretreatment with SU-88 prior to cimetidine resulted in a marked reduction in the lesions. SU-88 was found to increase the synthesis of gastric glycoproteins and to prevent the reduction of glycoprotein synthesis caused by the administration of absolute ethanol. However, no increase in the synthesis was observed 5 min after the SU-88 dosing, although the lesion was significantly suppressed at that time. These findings indicate that SU-88 possesses a cytoprotective effect and that this effect seems to be mediated by the increase in endogenous PG.

    Topics: Animals; Anti-Ulcer Agents; Cell Survival; Chalcone; Chalcones; Cimetidine; Dinoprostone; Ethanol; Gastric Mucosa; Glycoproteins; Hydrochloric Acid; Indomethacin; Male; Mucus; Propiophenones; Prostaglandins E; Rats; Rats, Inbred Strains; Stomach Ulcer

1984
Effects of sofalcone on necrotizing agents-induced gastric lesions and on endogenous prostaglandins in rats stomachs.
    Journal of pharmacobio-dynamics, 1984, Volume: 7, Issue:11

    Attempts were made to investigate the effect of 2'-carboxymethoxy-4,4'-bis(3-methyl-2-butenyloxy) chalcone (sofalcone) on necrotizing agents-induced gastric lesions and on prostaglandin E2 (PGE2)-like activity of the gastric tissue in rats. Sofalcone, 100 mg/kg i.p. and 300 mg/kg p.o., markedly suppressed 0.6 N HCl- or 100% EtOH-induced gastric lesions. Sofalcone, 100 mg/kg i.p., also significantly suppressed 0.2N NaOH-induced gastric lesions. Sofalcone suppressed 0.6 N HCl-induced gastric lesions with both oral and intraperitoneal routes, and the effect was particularly marked at 60 min. A dose of 100 mg/kg i.p. showed suppression lasting for up to 300 min. 0.6 N HCl-induced gastric lesions were significantly aggravated by indomethacin treatment (10 mg/kg s.c.). Oral sofalcone (300 mg/kg) significantly suppressed the aggravation of gastric lesions by indomethacin given before and after sofalcone, but the i.p. (100 mg/kg) did not show significant suppression in the case of pretreatment with indomethacin. PGs-like activity in the gastric tissue was increased in both of the fundus and the antrum by the administration of sofalcone without any dose-dependency. The increase was continuous and lasted for 6 h in the fundus of the stomach.

    Topics: Animals; Anti-Ulcer Agents; Chalcone; Chalcones; Dinoprostone; Gastric Mucosa; Indomethacin; Male; Necrosis; Propiophenones; Prostaglandins; Prostaglandins E; Rats; Rats, Inbred Strains; Stomach Ulcer; Time Factors

1984
Effect of an anti-ulcer agent, 2'-carboxymethoxy-4, 4'-bis (3-methyl-2-butenyloxy) chalcone (SU-88), on the biosynthesis of gastric sulfated mucosubstances in restrained and water-immersed rats.
    Japanese journal of pharmacology, 1984, Volume: 34, Issue:1

    2'-Carboxymethoxy-4,4'-bis(3-methyl-2-butenyloxy) chalcone (SU-88) has an anti-ulcer effect which is considered to increase the resistant factors of the gastric mucosa. In order to clarify the mechanism of the action of SU-88, the biosynthesis of gastric sulfated mucosubstances (SMS) in vivo and in vitro was investigated in rats with gastric erosion induced by restraint and water-immersion. The incorporation of 35S-sulfate into gastric SMS was significantly reduced 18 hr after the onset of stress. Pretreatment with SU-88 (500 mg/kg, p.o., X 10 days) prevented a reduction in the incorporation of 35S-sulfate due to stress when 35S-sulfate was administered in vivo. On the contrary, the incorporating activity of 35S-sulfate into the SMS in the isolated rat gastric mucosa with erosion was significantly increased 12 hr after the onset of stress, as compared with that of the control group in vitro. The incorporation of 35S-sulfate into the SMS was still further increased by the oral administration of SU-88. The mode of action of SU-88 on the biosynthesis of SMS was discussed.

    Topics: Animals; Anti-Ulcer Agents; Chalcone; Chalcones; Gastric Mucosa; Immersion; Male; Propiophenones; Rats; Rats, Inbred Strains; Restraint, Physical; Stomach Ulcer; Sulfates

1984