Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A decoction of Mikania cordata (Compositae) is commonly used for the treatment of gastric ulcer in the Rajbari district of Bangladesh. We have evaluated the anti-ulcerogenic effect of the alkaloidal fraction from the whole plant of M. cordata on diclofenac sodium-induced gastrointestinal lesion in rats. Long Evan's rats were divided into five groups. The control group was kept undisturbed. The vehicle group received vehicle after a 48-h fast. The diclofenac group received diclofenac sodium suspension (80 mg kg(-1)) after a 48-h fast. The diclofenac-ranitidine group (anti-ulcer drug used as a standard) received 35 mg kg(-1) ranitidine hydrochloride suspension 1 h after diclofenac sodium administration, after a 48-h fast. The diclofenac-extract group received alkaloidal fraction (50 mg kg(-1)) 1 h after diclofenac administration, after a 48-h fast. The biochemical, morphological and histological changes were studied. The data showed that the pH values of the stomach and duodenum were increased significantly (P < 0.001) in the alkaloidal-administered group compared with the control group (3.09 +/- 0.0429 vs 2.07 +/- 0.0339 and 6.79 +/- 0.1162 vs 6.19 +/- 0.1273, respectively). There were significant changes (P < 0.001) detected in the morphological study. The ulcer index of the stomach (0.268 +/- 0.0346) and of the duodenum (0.050 +/- 0.0129) in the alkaloidal-administered group were significantly lower than the diclofenac-only administered group (0.691 +/- 0.0184 and 0.0933 +/- 0.0138, respectively). According to the grading of tissue damage in the histological study, there were less or no lesions on the gastrointestinal mucosa of the alkaloidal-administered group compared with the diclofenac-only group (0 vs 5, respectively). When the results of the alkaloid extract group where compared with the ranitidine hydrochloride group a similar or more potent effect was observed with the alkaloidal extract group. The results of this study revealed that the bioactive principles of M. cordata have anti-ulcerogenic effects. The results validate the traditional use of this plant for the treatment of gastric ulcer in Bangladesh.
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PMID:The anti-ulcerogenic effect of an alkaloidal fraction from Mikania cordata on diclofenac sodium-induced gastrointestinal lesions in rats. 1104 98

Licorice, the root of Glycyrrhiza spp. (Fabaceae), has been used since ancient Egyptian, Greek, and Roman times in the West and since the Former Han era (the 2nd-3rd century B.C.) in ancient China in the East. In traditional Chinese medicine, licorice is one of the most frequently used drugs. In Japan, the oldest specimen of licorice introduced from China in the middle of the 8th century still exists in Shosoin, the Imperial Storehouse, in Nara. Extracts of licorice were recommended as a remedy for gastric ulcer by Revers of the Netherlands in 1946, which was soon withdrawn owing to its side effects. Carbenoxolon sodium, glycyrrhetinic acid (GA) hemisuccinate Na, was prepared from licorice to treat peptic ulcer in the UK. In Japan for the past 60 years, a glycyrrhizin (GL) preparation under the name of Stronger Neo-Minophagen C (SNMC) has been used clinically as an antiallergic and antihepatitis agent. GL and GA sometimes induce edema, hypertension, and hypokalemia in patients treated with higher doses and long-term administration. The mechanism of this side effect, pseudoaldosteronism, has been explained as due to the 11-hydroxy-steroid dehydrogenase inhibitory activity of GL and GA. The excess of endogenous cortisol produced combines with the renal mineral corticoid receptor, which promotes an aldosterone-like action. GL and GA reduce alanine transaminase (ALT) and aspartate transaminase (AST) values in the serum. This hepatoprotective effect has recently been explained as the inhibitory effects of GL and GA on immune-mediated cytotoxicity against hepatocytes and on nuclear factor (NF)-kappa B, which activates genes encoding inflammatory cytokines in the liver. To exclude the side effects and enhance the therapeutic activities, chemical modification of GL and GA has been performed. Deoxoglycyrrhetol (DG), homo- and heteroannular diene homologs of dihemiphthalates, showed a remarkable improvement in antiinflammatory, antiallergic, and antiulcer activities in animal experiments. Immunomodulating effects of GL, GA, and DG derivatives, which induce interferon-gamma and some other cytokines, have been demonstrated in relation with their antiviral activities. Antiinflammatory, antitumorigenic, and antimalarial effects of licorice flavonoids have also been investigated.
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PMID:A drug over the millennia: pharmacognosy, chemistry, and pharmacology of licorice. 1108 98

Recent studies demonstrated that experimental ulcers are associated with changes in the properties of voltage-sensitive sodium currents in sensory neurons. We hypothesized that nerve growth factor (NGF) contributes to these changes. Gastric ulcers were induced by acetic acid injection into the wall of the rat stomach. NGF expression was determined by ELISA and immunohistochemically. Sensory neurons were labeled by injection of a retrograde tracer into the gastric wall. Sodium currents were recorded in gastric sensory neurons from nodose and dorsal root ganglia cultured for 24 h in the presence of NGF or a neutralizing NGF antibody, respectively. Gastric ulcer formation caused a rise in NGF concentration within the gastric wall and an increase in NGF immunoreactivity. Exposure to NGF caused a significant increase in the TTX-resistant sodium current, whereas the TTX-sensitive sodium current remained unchanged. This was associated with an acceleration of the recovery from inactivation in spinal sensory neurons. Production and release of NGF in the gastric wall may contribute to sensitization of primary afferent neurons during gastric inflammation.
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PMID:Role of nerve growth factor in modulation of gastric afferent neurons in the rat. 1257 6

The maintenance of gastric mucosal function and integrity highly depends on the status of microcirculation. Vasoactive agents--prostaglandins, nitric oxide and sensory neuropeptides (e.g. calcitonin gene-related peptide)--play a crucial role in mucosal defensive processes. Beside the local release of vasoactive mediators the central nervous system is also involved in regulation of gastric functions. Cerebral lesions, stimulation of different brain areas can result in gastric mucosal injury. Noxious challenge of gastric mucosa alters the sodium currents in gastric sensory neurons and induces cfos mRNA expression in nucleus tractus solitarii and area postrema. Vagal nerve has long been established to play a permissive role in the development of gastric lesions. However, several lines of evidences suggest its physiological relevance in the enhancement of gastric mucosal resistance. It was concluded that gastroprotection can be induced by low level of central vagal stimulation and the consequent release of prostaglandins, nitric oxide, and calcitonin gene-related peptide. Prostaglandins, nitric oxide and sensory neuropeptides play a role also in ulcer healing by stimulating the formation of growth factors, the epithelial proliferation and angiogenesis. Both systemic and local administration of growth factors accelerated the ulcer healing. Local, single injection of plasmid-DNA encoding vascular endothelial growth factor (VEGF) was shown to stimulate the ulcer healing in the rat. The transient, local expression of VEGF in ulcerated tissue might be a new therapeutic strategy in the treatment of gastric ulcer disease.
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PMID:Gastric mucosal protection: from prostaglandins to gene-therapy. 1563 36

The gastroprotective activity of the diterpene ferruginol isolated from Prumnopitys andina wood and bark was determined on HCl/EtOH-induced gastric lesions in mice. The effect of the compound on the healing of subacute gastric lesions in rats was also studied. The mode of action of the diterpene was assessed using human gastric epithelial cells (AGS) and MRC-5 fibroblasts. The effect of ferruginol on the prostaglandin E2 content, protection against sodium taurocholate induced-damage and reduced glutathione content was evaluated on AGS cells as well as on the growth of AGS and fibroblast cultures. The free radical scavenging effect of ferruginol was assessed by the 1,1-diphenyl-2-picryl-hydrazil radical and superoxide anion assays. The effect of ferruginol on human erythrocyte membrane lipoperoxidation was determined. The cytotoxicity of the compound was assessed by means of the neutral red uptake. At 25 mg/kg, ferruginol inhibited the appearance of gastric lesions by 60% showing similar effects than lansoprazole at 20 mg/kg. Additionally, the compound displayed a significant ulcer healing activity in rats at 25 and 50 mg/kg with curative ratios of 36.0% and 92.5%, respectively, while the reference compound ranitidine at 50 mg/kg showed a curative ratio of 79.6%. At 6 and 12 microM, ferruginol increased significantly the prostaglandin E2 content. A strong inhibition of lipoperoxidation was found (IC50: 1.4 microM), but no effect was observed on the sodium taurocholate induced-damage or reduced glutathione content. Ferruginol stimulated cell proliferation at 1-2 microM in AGS cells and at 4-8 microM in fibroblasts, with cytotoxicities (IC50) of 24 and 26 microM, respectively. Our results support that ferruginol acts as gastroprotective increasing the PGs content, protecting the cells against lipid peroxidation and improving the gastric ulcer healing by a stimulating effect on the cell proliferation. These findings encourage further pharmacological studies of ferruginol as a potential new anti-ulcerogenic drug.
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PMID:Gastroprotective and ulcer healing effect of ferruginol in mice and rats: assessment of its mechanism of action using in vitro models. 1630 8

We clarified the roles of histamine H(1)-, H(2)-, H(3)-receptors and oxyradicals in the exacerbation of acid-induced gastric haemorrhage and stomach ulcer in endotoxaemic rats by measuring changes in gastric mucosal glutathione concentrations, lipid peroxide generation and histamine levels as well as in luminal electrolytes and haemoglobin contents. Stomach ulcers were evaluated by morphological and histological examination. Rats were deprived of food for 24 h, and challenged intravenously with lipopolysaccharide (LPS, 3 mg/kg) at 0, 12, 18 and 24 h after withdrawal of food. Control rats received saline only. Gastric truncal vagotomy was performed and followed by irrigation for 3 h with an acid solution containing 100 mmol/L HC1 and 54 mmol/L NaCl. The augmentation of mucosal permeability to electrolytes (acid back-diffusion), haemoglobin contents and lipid peroxide levels as well as the lowered mucosal glutathione concentrations were dependent on the duration of LPS intoxication. Serious damage of corpus mucosal cells was observed in acid-perfused stomachs of LPS rats. Intraperitoneal diphenhydramine, an H(1)-receptor antagonist, or ranitidine, an H(2)-receptor blocker, caused dose-dependent inhibition of these ulcerogenic factors. Antioxidants, including ascorbate and sodium benzoate, also were effective in inhibition. Moreover, intraperitoneal R-(alpha)-methylhistamine, an H(3)-receptor agonist, produced elimination, while thioperamide, an H(3)-receptor antagonist, and exogenous histamine elevated mucosal histamine concentrations and haemorrhagic ulcers in LPS rats. It is concluded that gastric haemorrhage and stomach ulcers produced by acid solution in LPS-treated rats are modulated by oxyradicals and histamine H(1)-, H(2)- and H(3)-receptors.
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PMID:Roles of histamine receptors and oxyradicals in aggravation of acid-induced gastric haemorrhagic ulcers in endotoxaemic rats. 1765 30

A gastroretentive drug delivery system of DA-6034, a new synthetic flavonoid derivative, for the treatment of gastritis was developed by using effervescent floating matrix system (EFMS). The therapeutic limitations of DA-6034 caused by its low solubility in acidic conditions were overcome by using the EFMS, which was designed to cause tablets to float in gastric fluid and release the drug continuously. The release of DA-6034 from tablets in acidic media was significantly improved by using EFMS, which is attributed to the effect of the solubilizers and the alkalizing agent such as sodium bicarbonate used as gas generating agent. DA-6034 EFMS tablets showed enhanced gastroprotective effects in gastric ulcer-induced beagle dogs, indicating the therapeutic potential of EFMS tablets for the treatment of gastritis.
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PMID:Gastroretentive drug delivery system of DA-6034, a new flavonoid derivative, for the treatment of gastritis. 1827 90

Byrsonima basiloba A. Juss. species is a native arboreal type from the Brazilian "cerrado" (tropical American savanna), and the local population uses it to treat diseases, such as diarrhea and gastric ulcer. It belongs to the Malpighiaceae family, and it is commonly known as "murici." Considering the popular use of B. basiloba derivatives and the lack of pharmacological potential studies regarding this vegetal species, the mutagenic and antimutagenic effect of methanol (MeOH) and chloroform extracts were evaluated by the Ames test, using strains TA97a, TA98, TA100, and TA102 of Salmonella typhimurium. No mutagenic activity was observed in any of the extracts. To evaluate the antimutagenic potential, direct and indirect mutagenic agents were used: 4 nitro-o-phenylenediamine, sodium azide, mitomycin C, aflatoxin B(1), benzo[a]pyrene, and hydrogen peroxide. Both the extracts evaluated showed antimutagenic activity, but the highest value of inhibition level (89%) was obtained with the MeOH extract and strain TA100 in the presence of aflatoxin B(1). Phytochemical analysis of the extracts revealed the presence of n-alkanes, lupeol, ursolic and oleanolic acid, (+)-catechin, quercetin-3-O-alpha-L-arabinopyranoside, gallic acid, methyl gallate, amentoflavone, quercetin, quercetin-3-O-(2"-O-galloyl)-beta-D-galactopyranoside, and quercetin-3-O-(2"-O-galloyl)-alpha-L-arabinopyranoside.
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PMID:Modulatory effect of Byrsonima basiloba extracts on the mutagenicity of certain direct and indirect-acting mutagens in Salmonella typhimurium assays. 1836 46

The purpose of this study was to test the hypothesis that sucralfate, a gastric ulcer medication, would alter plasma concentrations of total carbon dioxide (tCO2), lactate (LA), sodium (Na+), potassium (K+), chloride (Cl-) and total protein (TP), as well as calculated plasma strong ion difference (SID) and packed cell volume (PCV) in horses subjected to a simulated race test (SRT). Six unfit Standardbred mares (approximately 520 kg, 9-18 years) were used in a randomized crossover design with the investigators blinded to the treatment given. The horses were assigned to either a control (40-50 mL apple sauce administered orally (PO)) or a sucralfate (20 mg/kg bodyweight dissolved in 40-50 mL apple sauce administered PO) group. Each horse completed a series of SRTs during which blood samples were taken via jugular venipuncture at five sampling intervals (prior to receiving treatment, prior to SRT, immediately following exercise, and at 60 and 90 min post-SRT). During the SRTs, each horse ran on a treadmill fixed on a 6% grade for 2 min at a warm-up speed (4 m/s) and then for 2 min at a velocity predetermined to produce VO2max. Each horse then walked at 4 m/s for 2 min to complete the SRT. Plasma tCO2, electrolytes, LA, and blood PCV and TP were analysed at all intervals. No differences (P>0.05) were detected between control and sucralfate for any of the measured variables. There were differences (P<0.05) in tCO2, SID, PCV, TP, LA and electrolyte concentrations relative to sampling time. However, these differences were attributable to the physiological pressures associated with acute exercise and were not an effect of the medication. It was concluded that sucralfate did not alter plasma tCO2 concentration in this study.
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PMID:Effect of sucralfate on total carbon dioxide concentration in horses subjected to a simulated race test. 1895 Oct 51

The goal of the presented work was the research of signal transduction mechanism in the rat gastric parietal cells under stomach ulcer conditions. In these cells activation of adenylate cyclase (increase of cAMP level and proteinkinase A activity) and phosphoinositide (increases [Ca2+]i; cGMP and phoshatidylinocitole levels; proteinkinase C, proteinkinase G, and calmodulin-dependent-proteinkinase activity) of signals pathway was shown. An increase of plasma membrane phospholipids (PC, PS, PE, PI, LPC) level was shown. Under conditions of influence of the stress factor the membran enzymes activity (H+, K+ -ATPase, 5'-AMPase, Na+, K+ -ATPase, Ca2+, Mg2+ -ATPase and H+, K+ -ATPase) was considerably increased. The intensification of lipid peroxidation processes in rats was demonstrated.
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PMID:[Signal transudation pathways in parietal cells of the gastric mucosa in experimental stomach ulcer]. 1987 82


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