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1.  Antiulcer effect of the methanolic extract of Tamarindus indica seeds in different experimental models 
Peptic ulcer is a global health problem of the gastrointestinal tract characterized by mucosal damage secondary to pepsin and gastric acid secretion which occurs due to due to an imbalance between offensive and defensive factors.
The present study was carried out with methanolic extract of the seed coat of Tamarindus indica Linn. to evaluate its antiulcer potential on ibuprofen, alcohol and pyloric ligation induced gastric lesions.
Materials and Methods:
Doses of 100 mg/kg & 200 mg/kg of methanolic extract wre administered orally to rats of different groups. Ranitidine at a dose of 50 mg/kg was used as a standard drug for these gastric ulcer models. The gastric content was collected and the volume was measured. The ulceration index was determined by examining the inner lining of each stomach. Furthermore, the effect was assessed by free acidity, pepsin activity, total carbohydrate (TC), protein content (PK).
The result showed that the methanolic extract of seed coats of Tamarindus indica significantly reduce the total volume of gastric juice, free and total acidity of gastric secretion (P < 0.01) in pylorus ligation induced ulcer model as is comparable with the standard drug ranitidine. There was also a significant reduction in ulcer index (P < 0.01) as compared to control group.
The methanolic extracts of seed coat of Tamarindus indica can be used as a new source of antiulcer agent in animals.
PMCID: PMC3103918  PMID: 21687352
Peptic ulcer; ranitidine; Tamarindus indica; ulcer index
2.  Cytoprotective and Antioxidant Effects of the Methanol Extract of Eremomastax Speciosa in Rats 
Ethno-botanical information shows that Eremomastax speciosa is used in the traditional management of various stomach complaints including gastro-duodenal ulcers.
Materials and Methods
In this study, we tested the cytoprotective potential of the whole plant methanol extract (100–200 mg/kg, p.o), against HCl/ethanol, absolute ethanol, cold/restraint stress rats, and pylorus legated rats pre-treated with indomethacin. The effects of the extract on gastric lesion inhibition, the volume of gastric juice, gastric pH, gastric acid output, mucus production and gastric peptic activity were recorded. Oxidative stress parameters were measured in blood and gastric tissue samples obtained from the animals in all the models tested.
The extract significantly (p<0.05), reduced the formation of cold/restraint ulcers by (31–60%, inhibition), completely inhibited (100%) the formation of lesions induced by HCl/ethanol at the highest dose, but was less effective against absolute ethanol (22–46% inhibition). The extract (200 mg/kg), significantly reduced lesion formation (P<0.01), gastric acidity (P<0.01), and volume of gastric secretions (P<0.05), in the indomethacin/pylorus ligation model, and did not affect the activity of pepsin in gastric juice. Blood concentrations of antioxidant enzymes (catalase, SOD and GSH), increased significantly and MDA concentrations decreased in all models tested.
Cytoprotection by E. speciosa methanol extract was attributed to its ability to reduce acid secretion, and to enhance mucosal defence and in vivo antioxidant status.
PMCID: PMC3957260  PMID: 24653572
Eremomastax speciosa; cytoprotection; gastric ulcers; antioxidant status
3.  Serum carbenoxolone in patients with gastric and duodenal ulcer: Absorption, efficacy and side-effects. 
Gut  1978;19(4):330-335.
The absorption of carbenoxolone sodium has been studied in 15 patients with gastric ulcer and eight patients with duodenal ulcer treated for four weeks. Blood levels of carbenoxolone showed a log distribution, varied markedly between patients, and were significantly higher after Biogastrone tablets (300 mg/day) than after Duogastrone capsules (200 mg/day). Serum carbenoxolone levels were similar in patients taking Biogastrone tablets before or after meals, and in patients taking Biogastrone tablets or Duogastrone capsules with or without antacids following chronic administration. Serum carbenoxolone levels were similar in patients whose gastric ulcers had or had not healed after four weeks' treatment. Serum carbenoxolone was significantly higher in patients who developed oedema, and was significantly correlated with age and with fall in plasma potassium. Carbenoxolone may exert its metabolic effects systemically, but its ulcer-healing effects topically; additional studies are needed to test this hypothesis.
PMCID: PMC1411939  PMID: 648939
4.  Antiulcer Activity of Ethanolic Extract of Salvadora indica (W.) Leaves on Albino Rats 
Ulcer can be developed inside the inner lining of the stomach (gastric ulcer) or the small intestine (duodenal ulcer). Both the ulcers are also cumulatively referred as peptic ulcers. It affects nearly 10% of world population.
To investigate the antiulcer activity of ethanolic extract of Salvadora indica W. leaves (ESIL) on albino rats.
Materials and Methods
The present study was carried by pylorus ligation, ethanol and cysteamine induced ulcer models in albino rats. The antiulcer activity of ESIL (150, 300 and 600 mg/kg p.o. for 7 days) was compared with standard drugs (Ranitidine). In pyloric ligation induced ulcer model, the studied parameters were gastric volume, pH, total acidity, free acidity, and ulcer index whereas in ethanol and cysteamine induced ulcer model, the ulcer index was determined for severity of ulcers. The parameters studied were ulcer index, gastric juice volume, pH, free acidity and total acidity.
In pyloric ligation model; the volume of gastric content, total/free acidity and pepsin activity was significantly decreased at p<0.05 and p<0.01 and pH of the gastric juice was significantly increased at p<0.05 and p<0.01 in ESIL treated groups as compared to control group. All the doses of ESIL showed dose dependent antiulcer effect as well as significant (p<0.05 and p<0.01) reduction in the ulcer index as compared to control group in all the experimental models.
The results of the study indicate that the ESIL have better potential against ulcer which supports the traditional claims in folklore medicine.
PMCID: PMC5071962  PMID: 27790462
Antiulcer effect; Cysteamine; Ethanol; Pylorus ligation; Ulcer index
5.  Ulcer Protective Activity of Jatropha gossypiifolia Linn. in Wistar Rats 
Pharmacognosy Research  2016;8(Suppl 1):S61-S66.
Several synthetic drugs are useful in the treatment of peptic ulcer, but almost of these drugs are used in prolonging time, it may cause several adverse reactions. However, the herbal medicines are more potent to the treatment and minimize the side effects.
To evaluate the methanol extract of Jatropha gossypiifolia Linn. (MEJG) for gastro protective activity against Wistar rats.
Materials and Methods:
Anti-ulcer potency of MEJG (100 and 200 mg/kg, b.w.) was assessed using aspirin (200 mg/kg, p.o.) plus pylorus ligation ulcer model and the parameters studied were ulcer index (UI), gastric juice volume, pH, total acidity, and total acid output. Same extract was studied by ethanol-induced (80%, 5 mL/kg, intragastrically) ulcer model, and the UI and biochemical parameters were studied.
The oral administration of MEJG (100 and 200 mg/kg) significantly (P < 0.001) attenuated the ulcer score and anti-secretary parameters (such as the volume of gastric content, free acidity, total acidity, and total acid output) in the aspirin plus pylorus ligation rats. The extract also significantly attenuated (P < 0.001) ulcer score in ethanol-induced ulcer model and lipid peroxidation level and significantly increased the level of glutathione peroxides, catalase, and superoxide dismutase activity. The MEJG may possess active constituents such as alkaloids, glycosides, flavonoids, and terpenes, which may play a major role in gastroprotective effect in Wistar rats.
The present study provides scientific support for the anti-ulcer activities of extracts of JG and also claimed that antioxidant potential of the extracts. However, substantiates the traditional claims for the usage of this drug in the treatment of gastric ulcer.
The methanolic extract of jatropha gossypiifolia Linn. for gastro protective activity against aspirin plus pyloric ligation and ethanol induced ulcer models was studied in Wistar rats. JG shows significantly attenuated the ulcer score in both models. And also attenuated in anti-secretory parameters in aspirin induced ulcer model. MEJG may possess active constituents such as alkaloids, glycosides, flavonoids and terpenes, which may play a major role in gastroprotective effect in Wistar rats.
Abbreviation Used: MEJG: Methanolic extract of jatropha gossypiifolia, mg: Milli gram, kg: Kilogram, b.w.: Body weight, p.o.: Per oral, UI: Ulcer index, pH: Concentration of H+ ion, mL: Milli litre, JG: Jatropha gossypiifolia,USD: United States Dollar, NSAIDs: Non steroidal anti-inflammatory drugs, v/v: Volume by volume, w/v: Weight by volume, SCMC: Sodium carboxy methyl cellulose, g: Gram, h: Hour, °C: Degree centigrade, n: Number, Rpm: Rotation per minute, Min: Minute, N: Normality, NaoH: Sodium hydroxide, mM - Millimole, TBA: Thiobarbituric acid, nmol: Nanomole, nm: Nanometer, GPx: Glutathione peroxidase, GSH: Reduced glutathione, H2O2: Hydrogen peroxide, SOD: Superoxide dismutase, ANOVA: Analysis of Variance, μmol: Micromole
PMCID: PMC4821110  PMID: 27114695
Antioxidant enzymes; anti-ulcer; aspirin; ethanol; jatropha gossypiifolia; ranitidine; wistar rats
6.  pH, healing rate, and symptom relief in patients with GERD. 
Gastroesophageal reflux symptoms are common and occur in all of us from time to time. In others, reflux may be associated with ulcerative esophagitis. The symptoms may be aggravated by large meals, coffee, smoking and position. Physiological and pathological reflux can be separated by the frequency and duration of the exposure of the lower esophagus to acid. Pathological reflux results in symptoms and also esophagitis and ulceration in some patients. Although gastroesophageal reflux disease (GERD) is considered to result from a disorder of motility in the esophagus, gastric acid and peptic activity are deemed pivotal to the initiation and continuation of the esophageal damage and the development of symptoms. Acid exposure in the esophagus is normally less than 4 percent of the 24 hours with a pH below 4. An increase over 4 percent of the time with a pH less than 4 is considered pathological. Hence, antisecretory drugs have become the principle approach to the treatment of reflux symptoms and esophagitis since they reduce the acidity, of gastric juice and the activity of pepsin. Importantly, they also reduce the volume of gastric juice available for reflux into the esophagus. There is a clear relationship between the degree and duration of acid suppression and the relief of heartburn and healing of esophagitis. Pharmacodynamic studies with different dose regimens of the H2-receptor antagonists and the proton pump inhibitors show a difference in the degree and duration of the antisecretory effect, and this correlates closely with the results of clinical trials with respect to the healing of esophagitis and the relief of symptoms. Proton pump inhibitors achieve healing rates by week four, which are not achieved by H2-receptor antagonists even after 12 weeks of treatment. The advantage of proton pump inhibitors over H2-receptor antagonists is due to the greater degree, longer duration of effect and more complete inhibition of acid secretion that maintains intragastric pH above 4 for a maximal duration. Although there is no significant difference between proton pump inhibitors with respect to healing of esophagitis, symptom relief occurs earlier with lansoprazole than omeprazole, and this is probably due to the greater oral bioavailability and faster onset of action of lansoprazole when compared to omeprazole.
PMCID: PMC2579003  PMID: 10780580
7.  Mucus degradation by pepsin: comparison of mucolytic activity of human pepsin 1 and pepsin 3: implications in peptic ulceration. 
Gut  1986;27(3):243-248.
The ability to digest mucus, mucolytic activity of isolated pepsins and samples of human gastric juice has been assayed by measuring the fall in viscosity when incubated with purified pig gastric mucus glycoprotein. Pure human pepsin 1, the peptic ulcer associated pepsin, digested gastric mucus glycoprotein at a faster rate than did pure human pepsin 3 (the principal human pepsin), or the equivalent pig pepsin (pepsin A). At pH 2.0 pepsin 1 had twice the mucolytic activity of pepsin 3. Above pH 3.8 this difference became more marked and whereas pepsin 1 caused substantial mucolysis up to and including pH 5.1, pepsin 3 had minimal activity. At pH 4.0 pepsin 1 had six times the mucolytic activity of pepsin 3. Gastric juices from patients with duodenal ulcer each exhibited substantial mucolytic activity between pH 2 to 5, similar to that of pepsin 1. In contrast, gastric juice from non-symptomatic volunteers exhibited little mucolytic activity above pH 4. Analysis of the mucus glycoprotein by gel filtration showed that an increase in lower molecular weight, pepsin degraded, glycoprotein was associated with the fall in mucus viscosity for all enzyme preparations. These results showed that pepsin 1 can digest the mucus more effectively than pepsin 3 and at higher pH values. The raised concentrations of pepsin 1 in the juice of peptic ulcer patients may thus promote the ulcerative process by increased erosion of the mucus barrier under conditions likely to pertain in the duodenal bulb as well as the stomach.
PMCID: PMC1433406  PMID: 3084340
8.  11β-hydroxysteroid dehydrogenase inhibition as a new potential therapeutic target for alcohol abuse 
Translational Psychiatry  2016;6(3):e760-.
The identification of new and more effective treatments for alcohol abuse remains a priority. Alcohol intake activates glucocorticoids, which have a key role in alcohol's reinforcing properties. Glucocorticoid effects are modulated in part by the activity of 11β-hydroxysteroid dehydrogenases (11β-HSD) acting as pre-receptors. Here, we tested the effects on alcohol intake of the 11β-HSD inhibitor carbenoxolone (CBX, 18β-glycyrrhetinic acid 3β-O-hemisuccinate), which has been extensively used in the clinic for the treatment of gastritis and peptic ulcer and is active on both 11β-HSD1 and 11β-HSD2 isoforms. We observed that CBX reduces both baseline and excessive drinking in rats and mice. The CBX diastereomer 18α-glycyrrhetinic acid 3β-O-hemisuccinate (αCBX), which we found to be selective for 11β-HSD2, was also effective in reducing alcohol drinking in mice. Thus, 11β-HSD inhibitors may be a promising new class of candidate alcohol abuse medications, and existing 11β-HSD inhibitor drugs may be potentially re-purposed for alcohol abuse treatment.
PMCID: PMC4872439  PMID: 26978742
9.  Evaluation of Antiulcer and Antioxidant Activity of Barleria gibsoni Dalz. Leaves 
Pharmacognosy Research  2016;8(4):226-230.
Peptic ulcer is a digestive disorder most commonly found in clinical practice. Given the many side effects of modern medicine, the initial acquisition of fewer side effects, and medication of indigenous drugs, it should be considered as a better alternative for the treatment of peptic ulcer.
To assess antiulcer and antioxidant activity of ethanol extract of Barleria gibsoni (EBG) Dalz. leaves in ulcer-induced rats and in vitro antioxidants method, respectively.
Materials and Methods:
Ethanol EBG was screened for antiulcer activity in pylorus ligation-induced ulcer models in Wistar rats. In vitro antioxidant activity of the extracts was tested using 2,2-diphenyl-1-picrylhydrazyl (DPPH), nitric oxide (NO) radical scavenging activity. Total phenol and flavonoid content in the extracts were determined spectrophotometrically.
Oral administration of ethanol extract of leaves at doses of 250, 500 mg/kg p.o. reduced significant gastric lesions induced by pylorus ligation-induced ulcer as compared to standard omeprazole (20 mg/kg p.o.). The IC50 values were found to be 150 μg/mL in leaves extract. The ethanol extracts showed good antioxidant capacity in DPPH radical scavenging assay and NO radical scavenging activity when compared to standard. The total phenolic content using Folin–Ciocalteu reagent estimated in 1 mg of leaves extracts was 368 μg and 481 μg with gallic acid equivalent and also the total flavonoid content found to be 240 and 410 μg, respectively, with quercetin equivalence.
These findings suggest that the leaves of B. gibsoni possessed antiulcer potential and antioxidant compared to standard. This is the first ever report of antiulcer and antioxidant activities in B. gibsoni (Acanthaceae).
In vivo antiulcer and in vitro antioxidant activity of Barleria gibsoni was evaluated.Soxhelt extraction was carried out and extracts were subjected to qualitative phytochemical analysis. Extract obtained by Soxhlation showed higher total phenolic and flavonoid contents.EBG showed DPPH and Nitric oxide scavenging activity indicating its strong antioxidant potential.On pylorus ligation-accumulated secretions and the related ulcers confirm gastric acid output to be the basic cause of gastric ulcers. Ethanol extract of leaves attenuated the gastric volume, free acidity, total acidity and ulcer index thus showing the anti-secretory mechanism.The results of the histopathological investigation of Barleria gibsoni leaves for antiulcer effects using pylorus ligation induced ulcer model in rats laid credence to traditional use of the plant leaves in ulcer treatment. The ethanol extract of leaves demonstrated increase in percentage preventive index compared to omeprazole respectively. From the present study results reveals the antiulcer activity of ethanol extract leaves which is comparable to that of Omeprazole.
Abbreviations Used: EBG: Ethanol extract prepared from the leaves of B. gibsoni, ROS: Reactive Oxygen Species, DPPH: 2, 2-diphenyl-1-picrylhydrazyl, NO: Nitric Oxide, IC50: The half maximal inhibitory concentration, m: mg, DNA: deoxyribonucleic acid, GAE: Gallic acid equivalence, AlCl3: Aluminium chloride
PMCID: PMC5004510  PMID: 27695259
Acanthaceae; Barleria gibsoni; gallic acid; L-ascorbic acid; pylorus ligation-induced ulcer model; quercetin
10.  The evaluation of anti-ulcerogenic effect of rhizome starch of two source plants of Tugaksheeree (Curcuma angustifolia Roxb. and Maranta arundinacea Linn.) on pyloric ligated rats 
Ayu  2014;35(2):191-197.
In the present era, because of the life-style, the disorders such as hyperacidity and gastric ulcers are found very frequently. Satwa (starch) obtained from the rhizomes of two plants namely Curcuma angustifolia Roxb. and Maranta arundinacea Linn. are used in folklore practice for the treatment of above complaints under the name Tugaksheeree.
To compare the anti-ulcerogenic activity of the above two drugs in pyloric ligation induced gastric ulcer in albino rats.
Materials and Methods:
A total of 18 Wistar strain albino rats of both sexes grouped into three groups. Group C served as pyloric ligated control group, Group I received starch of C. angustifolia suspension and Group II received starch of M. arundinacea for seven days. On 8th day pylorus was ligated. After ligation the animals were deprived of food and water and sacrificed at the end of 14 h. The collected gastric contents were used for biochemical estimation and ulcer index was calculated from excised stomach.
Both the test drugs showed statistically significant decrease in the volume, increase in the pH, reduced the free acidity of gastric juice and decreased the peptic activity. The starch of C. angustifolia reduced a total acidity non-significantly while M. arundinacea reduced it significantly. Among the two drugs the M. arundinacea has effectively reduced the peptic activity, which is statistically significant. M. arundinacea shown statistically significant increase of total carbohydrates.
Both the test drugs proved anti-ulcer activity and prevents the chance of gastric ulcer. Among these two M. arundinacea is more effective.
PMCID: PMC4279328  PMID: 25558167
Curcuma angustifolia; gastric ulcer; Maranta arundinacea; pyloric ligation; starch; Tugaksheeree
11.  Clinical trial of a new carbenoxolone analogue (BX24), zinc sulphate, and vitamin A in the treatment of gastric ulcer 
Gut  1972;13(6):459-463.
The effects of a new carbenoxolone analogue (BX24), zinc sulphate, and vitamin A on the healing of gastric ulcer have been assessed in a multifactorial clinical trial conducted in out-patients treated for four weeks.
Forty-eight patients completed the trial. Three groups of eight patients were given respectively 300, 600, and 1 200 mg of BX24 daily and were compared with 24 patients who were given 300 mg of carbenoxolone sodium daily. The size of the ulcer niche was reduced on average by 14·6% in the eight patients given BX24 300 mg daily, by 47·6% in the patients given 600 mg daily, and by 51·0% in the patients given 1 200 mg daily. In the patients given carbenoxolone the size of the niche was reduced by 68·9%. These results were compared with those obtained previously with carbenoxolone and inert tablets and it was concluded that BX24 is without clinically useful effect in the doses used.
Eleven of the 24 patients (46%) treated with carbenoxolone sodium developed side effects due to fluid retention and electrolyte disturbances. None of the patients given BX24 experienced such effects.
In addition to carbenoxolone or BX24, 24 patients were given zinc sulphate, 660 mg daily, and in 24 patients these tablets were withheld. Among the patients given carbenoxolone the reduction in the size of the niche was much the same irrespective of whether or not the patients received zinc sulphate. Among the 12 patients given BX24 with zinc sulphate the ulcer healed completely in four and, on average, the size of the niche was reduced by 53·5%, compared with 21·9% in the 12 patients given BX24 alone. This difference is not statistically significant but the possibility of a beneficial effect from zinc is not excluded. No side effects attributable to zinc were observed.
Twenty-four patients were also given vitamin A, 50 000 units daily, and in 24 patients the vitamin was withheld. No evidence was obtained to suggest that vitamin A had any beneficial effect on the healing of gastric ulcer.
PMCID: PMC1412200  PMID: 4557308
12.  Metabolic Studies, Aldosterone Secretion Rate, and Plasma Renin after Carbenoxolone Sodium 
British Medical Journal  1969;2(5660):793-795.
A formal metabolic study of carbenoxolone sodium (Biogastrone) 300 mg./day has been performed for 17 days on a woman with gastric ulcer who in a previous 21-day trial, on a 52-mEq sodium diet, showed weight gain, retention, and rise in plasma sodium and chloride concentrations, as well as hypokalaemia without change in potassium balance. In the present trial sodium intake was restricted to 26 mEq/day; while plasma electrolyte changes of lesser degree still occurred, there was no retention of water, sodium, or chloride. Aldosterone secretion in the control period was 202 μg./24 hours, and fell to 74 μg./24 hours after carbenoxolone, but plasma renin was unchanged.
These results suggest that the mineralocorticoid effects of carbenoxolone (and presumably of liquorice and its other derivatives) are due to an intrinsic aldosterone-like action, and that, with sodium deprivation, aldosterone secretion is suppressed by a mechanism which is not renin-mediated—possibly hypokalaemia.
PMCID: PMC1983758  PMID: 5784614
13.  Gastric epithelial cell turnover, mucus production, and healing of gastric ulcers with carbenoxolone. 
Gut  1977;18(10):817-820.
Nineteen healthy subjects were studied and 17 patients with gastric ulcer before and after ulcer healing with carbenoxolone. Gastric deoxytibonucleic acid (DNA) loss was measured as an index of epithelial cell turnover, and N-acetylneuraminic acid (NANA) content of gastric juice as an index of mucus secretion. In normal subjects there was a negative correlation (p less that 0-025) between gastric DNA loss and NANA secretion; the lower the cell turnover the higher the NANA production. In gastric ulcer patients DNA loss or turnover was significantly (p less than 0-01) higher than normal, and fell significantly (p less than 0-01) after four weeks' treatment with carbenoxolone when 16 of the 17 ulcers had healed. At the same time NANA output increased significantly (p less than 0-01). It is suggested that patients with gastric ulcer lose cells at a high rate, a state of affairs which is returned towards normal by carbenoxolone, thus allowing the epithelial cells to mature within the mucosa and produce more mucus.
PMCID: PMC1411689  PMID: 590840
14.  Effects of beta-adrenoceptor drug stimulation on various models of gastric ulcer in rats. 
British Journal of Pharmacology  1982;76(4):587-594.
1. Experiments were designed to evaluate the effect of the pharmacological activation of beta-adrenoceptors on various models of gastric ulcer in the rat. 2. Pretreatment with the beta-adrenoceptor stimulant drugs, isoprenaline or salbutamol, significantly inhibited stress-induced gastric ulcers. This anti-ulcer effect was abolished by propranolol but not by atenolol, suggesting that beta 2-adrenoceptors mediate this response. 3. In the pylorus-ligation model, salbutamol inhibited lesion formation and reduced the intragastric content of hydrogen ions, histamine and pepsin although the latter was only affected with the higher dose of salbutamol. 4. Salbutamol also prevented the ulcerogenic action on the gastric mucosa of an exogenously perfused artificial gastric juice, showing that the anti-ulcer effect is not necessarily dependent on acid inhibition. 5. Salbutamol also reduced the formation of acute ulcers induced by various iatrogenic means (histamine, polymyxin B, reserpine and indomethacin). 6. Long-term treatment with salbutamol accelerated the healing of experimental chronic gastric ulcer. 7. In anaesthetized rats, salbutamol produced a dose-related increase in mucosal blood flow which may contribute to its mode of action. 8. It is concluded that beta-adrenoceptor agonists exert preventive and curative effects on gastric damage induced in the rat. This effect seems specific and mediated through beta-adrenoceptor activation.
PMCID: PMC2071816  PMID: 6125225
15.  Pepsin 1 secretion in chronic peptic ulceration. 
Gut  1980;21(9):766-771.
In patients with peptic ulceration, both vagal stimulation by insulin hypoglycaemia and stimulation by pentagastrin cause pepsin 1 to be secreted into gastric juice. There is a secretory threshold for pepsin 1, below which only pepsins 3 and 5 are secreted. Pepsin 1 accounts for an increasing proportion of the total peptic activity/ml of gastric juice as the total activity increases. Higher concentrations of pepsin 1 in the basal gastric secretion occurred significantly more frequently in patients with duodenal ulcer than with gastric ulcer. In these patients there may be an increased 'background' secretory drive.
PMCID: PMC1419519  PMID: 6776016
16.  Role of nitrite, urate and pepsin in the gastroprotective effects of saliva 
Redox Biology  2016;8:407-414.
Dietary nitrate is now recognized as an alternative substrate for nitric oxide (•NO) production in the gut. This novel pathway implies the sequential reduction of nitrate to nitrite, •NO and other bioactive nitrogen oxides but the physiological relevance of these oxidants has remained elusive. We have previously shown that dietary nitrite fuels an hitherto unrecognized nitrating pathway at acidic gastric pH, through which pepsinogen is nitrated in the gastric mucosa, yielding a less active form of pepsin in vitro. Here, we demonstrate that pepsin is nitrated in vivo and explore the functional impact of protein nitration by means of peptic ulcer development. Upon administration of pentagastrin and human nitrite-rich saliva or sodium nitrite to rats, nitrated pepsin was detected in the animal's stomach by immunoprecipitation. •NO was measured in the gastric headspace before and after nitrite instillation by chemiluminescence. At the end of each procedure, the stomach's lesions, ranging from gastric erosions to haemorrhagic ulcers, were scored. Nitrite increased gastric •NO by 200-fold (p<0.05) and nitrated pepsin was detected both in the gastric juice and the mucosa (p<0.05). Exogenous urate, a scavenger of nitrogen dioxide radical, blunted •NO detection and inhibited pepsin nitration, suggesting an underlining free radical-dependent mechanism for nitration. Functionally, pepsin nitration prevented the development of gastric ulcers, as the lesions were only apparent when pepsin nitration was inhibited by urate. In sum, this work unravels a novel dietary-dependent nitrating pathway in which pepsin is nitrated and inactivated in the stomach, preventing the progression of gastric ulcers.
Graphical abstract
•The nitrate-nitrite-nitric oxide pathway promotes gastric protein nitration.•Pepsin is nitrated by dietary nitrite through the production of ∙NO2.•Nitrated pepsin prevents the development of acute peptic ulcers.
PMCID: PMC4864375  PMID: 27156250
Nitrate; Nitrite; Tyrosine nitration; Stomach
17.  Gastroprotective and Ulcer Healing Effects of Essential Oil of Hyptis martiusii Benth. (Lamiaceae) 
PLoS ONE  2014;9(1):e84400.
Hyptis martiusii Benth. is an aromatic plant found in abundance in northeastern Brazil that is used in ethnomedicine to treat gastric disorders. The aim of this study was to elucidate the mechanisms of action involved in the gastroprotection of the essential oil of Hyptis martiusii (EOHM) and to evaluate its healing capacity. Wistar rats were exposed to different protocols and subsequently were treated with 1% Tween-80 aqueous solution (negative control), pantoprazole, carbenoxolone, N-acetylcysteine (depending on the specificity of each model) or EOHM. The antisecretory activity (basal or stimulated) was determined using the pyloric ligature method. The gastroprotective action of nitric oxide and sulphydryl groups (–SH groups), as well as the quantification of adherent mucus and the levels of malondialdehyde and –SH groups in gastric mucosa, were evaluated using ethanol-induced gastric ulcer model. The healing ability was evaluated using the acetic acid-induced gastric ulcer model and histological and immunohistochemical analysis (HE, PAS and PCNA). EOHM (400 mg/kg) reduced the volume and acidity of gastric secretion stimulated by histamine and pentagastrin. The gastroprotective effect of EOHM involves the participation of endogenous sulfhydryl groups. EOHM increased mucus production (54.8%), reduced levels of MDA (72.5%) and prevented the depletion of –SH groups (73.8%) in the gastric mucosa. The treatment with EOHM reduced in 70.3% the gastric lesion area, promoting significant regeneration of the gastric mucosa, as confirmed by histological analysis and analysis of proliferating cell nuclear antigen. The results show that gastroprotective effect of EOHM is mediated by cytoprotective and antioxidant mechanisms and by their antisecretory activity, and suggest that the essential oil of Hyptis martiusii is a promising candidate for the treatment of gastric ulcers.
PMCID: PMC3893125  PMID: 24454726
18.  Pepsin 5 in gastric juice: determination and relationship to the alkali-stable peptic activity. 
Gut  1979;20(11):977-982.
Pure human pepsins 1 and 3 are inactivated by incubation at pH 7.1-7.3 for 30 minutes, losing 90% or more of activity. Pepsin 5 is alkali-stable, retaining 100% of activity. Mixtures of pure pepsins 1 and/or 3 with pepsin 5 were found to have greater alkali-stable activity than predicted. Two published methods for determining the alkali-stable fraction of the peptic activity of gastric juice gave, respectively, in our hands values of 45.4-80.0% and 27.5-43.9% of the total activity. These values seemed too high to be attributable only to pepsin 5 in gastric juice, as agar gel electrophoresis shows pepsin 3 to have the principal activity. Electrophoretograms of alkaline incubated gastric juice revealed that large amounts of pepsin 3 retained activity as well as pepsin 5, and a proteolytic zone "4" appeared between them. Alkali inactivation thus does not allow the estimation of pepsin 5 individually in gastric juice. Pepstatin, at a final concentration of 100 to 170 pmol/ml, may be used to estimate pepsin 5 in gastric juice and gave values of 18.0 to 27.6% of the total peptic activity. Pepsin 5, in gastric juice and in mixtures of pepsins, appears to protect pepsin 3 from alkaline-inactivation, and to a lesser extent from pepstatin inhibition.
PMCID: PMC1412680  PMID: 43273
19.  A potential of some medicinal plants as an antiulcer agents 
Pharmacognosy Reviews  2010;4(8):136-146.
Peptic ulcers are a broad term that includes ulcers of digestive tract in the stomach or the duodenum. The formation of peptic ulcers depends on the presence of acid and peptic activity in gastric juice plus a breakdown in mucosal defenses. There are two major factors that can disrupt the mucosal resistance to injury: non-steroidal antiinflammatory drugs (NSAIDs) example, aspirin and Helicobacter pylori infection. Numerous natural products have been evaluated as therapeutics for the treatment of a variety of diseases, including peptic ulcer. There has been considerable pharmacological investigation into the antiulcer activity of some compounds. In this work, we shall review the literature on different medicinal plant and alkaloids with antiulcer activity. This article reviews the antiacid/anti-peptic, gastroprotective and/or antiulcer properties of the most commonly employed herbal medicines and their identified active constituents. The experimental parameters used for antiulcer activity were cold restraint stress-induced ulcer model, Diclofenac-induced ulcer model in rats, (HCl–ethanol)-induced ulcer in mice and water immersion stress-induced ulcer in rats. The ideal aims of treatment of peptic ulcer disease are to relieve pain, heal the ulcer and delay ulcer recurrence. About 70% of patients with peptic ulcer disease are infected by Helicobacter pylori and eradication of this microorganism seems to be curative for this disease. This article reviews drugs derived from medicinal plant more commonly used in the world for peptic ulcer and, if reported, the antiulcer activity. This article will be concerned only with the antiulcer and gastro-protective effects.
PMCID: PMC3249913  PMID: 22228953
Alkaloids; antiulcer activity; flavonoids; peptic ulcer; saponin; tannins
20.  Evaluation on the Pharmacological Effect of Traditional Chinese Medicine SiJunZiTang on Stress-Induced Peptic Ulcers 
Purpose. To explore the effects of SiJunZiTang (SJZT) on central neurotransmitters and the inhibition of HCl hypersecretion, along with the role of the vagus nerve. From this, the effects of SJZT and its constituent ingredients on inhibiting stress-induced peptic ulcers will be determined. Methods. Methods used to determine SJZT's effectiveness included (1) measuring the antipeptic ulcer effects of varying combinations of the constituents of SJZT; (2) evaluations of monoamine (MA) level in the brain; and (3) measuring the effects of longer-term SJZT treatment. Results. Comparing the control and experimental groups where the rats' vagus nerves were not cut after taking SJZT orally (500 mg/kg and 1000 mg/kg), the volume of enterogastric juice, free HCl and total acidity all reduce dose-dependently. The group administered SJZT at 1000 mg/kg showed significant reductions (P < 0.05). For the experimental groups where the vagus nerves were cut, a comparison with the control group suggests that the group receiving SJZT (500 mg/kg) orally for 21 days demonstrated a cure rate of 34.53%. Conclusion. The results display a correlation between the therapeutic effects of SJZT on stress-induced peptic ulcers and central neurotransmitter levels. Further to this, SJZT can inhibit the hypersecretion of HCl in the stomach, thus inhibiting stress-induced peptic ulcers.
PMCID: PMC3694386  PMID: 23840247
21.  Comparative Study of Proton Pump Inhibitors on Dexamethasone Plus Pylorus Ligation Induced Ulcer Model in Rats 
The present study was designed to compare ulcer protective effect of proton pump inhibitors viz. omeprazole, rabeprazole and lansoprazole against dexamethasone plus pylorus ligation induced ulcer model. Dexamethasone (5 mg/kg) was used as an ulcerogen. Dexamethasone suspended in 1% CMC in water was given orally to all the rats 15 min after the pylorus ligation. Omeprazole (20 mg/kg), rabeprazole (20 mg/kg), and lansoprazole (20 mg/kg) were administered by oral route 30 min prior to ligation was used for ulcer protective studies, gastric secretion and mucosal studies. Effects of proton pump inhibitors were determined by the evaluation of various biochemical parameters such as ulcer index, free and total acidity, gastric pH, mucin, pepsin and total proteins. Oral administration of proton pump inhibitors showed significant reduction in gastric acid secretion and ulcer protective activity against dexamethasone plus pylorus ligation induced ulcer model. The % protection of omeprazole, rabeprazole and lansoprazole was 84.04, 89.36 and 79.78, respectively. Rabeprazole significantly inhibited the acid-pepsin secretion and increased the gastric mucin secretion. The observations made in the present study suggest that rabeprazole is the most effective gastric antisecretory and ulcer healing agent as compared to omeprazole and lansoprazole.
PMCID: PMC3003173  PMID: 21188049
Dexamethasone; PPIs; mucosal offensive and defense factors
22.  Protective effect of hydro-alcoholic extract of Ruta graveolens Linn. leaves on indomethacin and pylorus ligation-induced gastric ulcer in rats 
The search for an ideal and new antiulcer drug has been extended to herbals for novel molecules that decrease the incidence of relapse and afford better protection.
The present study was designed to investigate the protective effect of hydro-alcoholic extract of Ruta graveolens (RGE) Linn. leaves on indomethacin (IND) and pylorus ligation-induced gastric ulcer in Wistar rats.
Materials and methods
The rats of all the six groups were deprived of food for 24 h. Then, the first group received 1 ml/kg/day p.o. of 1% carboxymethylcellulose calcium (CMC), second group 1 ml/kg/day p.o. of 1% CMC and third group 20 mg/kg/day p.o. of IND. Fourth and fifth groups received RGE 200 and 400 mg/kg/day p.o., respectively; while the sixth group 10 mg/kg/day p.o. omeprazole. After 30 min, last three groups received 20 mg/kg/day p.o. of IND also. All these treatments after food deprivation were repeated each day for 5 consecutive days. Pylorus ligation was performed on 6th day in last five groups. After 4 h, stomach by sacrifice of the rats was examined for ulcer index (UI) and gastric mucus. Gastric juice was assessed for acidity, pH and pepsin; while gastric tissues were assessed for thiobarbituric acid reactive substance (TBARS) and glutathione (GSH).
Fifth group showed significant decrease in UI (10.33 ± 0.67), TBARS (0.33 ± 0.03 mmol/mg), free acidity (48.78 ± 5.12 meq/l/100 g), total acidity (99.33 ± 9.31 meq/l/100 g), and pepsin activity (8.47 ± 0.41 μg/ml) levels while it showed significant increase in mucus (412.4 ± 21.6 μg/g), GSH (57.9 ± 4.8 mmol/mg) and pH (3.32 ± 0.27) compared to third group. Percent protection in RGE 400 mg was found to be 63.32 compared to indomethacin.
RGE possesses antiulcerogenic activity as it exhibits protective effect on gastric ulcer in rats.
PMCID: PMC4910575  PMID: 27297508
Glutathione; Protective activity; Ruta graveolens; Thiobarbituric acid reactive substance; Ulcer index
California Medicine  1949;70(1):10-15.
Thirteen patients with peptic ulcer were treated with fresh cabbage juice, which, experiments have indicated, contains an antipeptic ulcer factor. This factor (vitamin U) prevents the development of histamin-induced peptic ulcers in guinea pigs.
The average crater healing time for seven of these patients who had duodenal ulcer was only 10.4 days, while the average time as reported in the literature, in 62 patients treated by standard therapy, was 37 days.
The average crater healing time for six patients with gastric ulcer treated with cabbage juice was only 7.3 days, compared with 42 days, as reported in the literature, for six patients treated by standard therapy.
The rapid healing of peptic ulcers observed radiologically and gastroscopically in 13 patients treated with fresh cabbage juice indicates that the anti-peptic ulcer dietary factor may play an important role in the genesis of peptic ulcer in man.
PMCID: PMC1643665  PMID: 18104715
24.  Clot lysis by gastric juice: an in vitro study. 
Gut  1989;30(12):1704-1707.
Gastric juice from patients with peptic ulcer disease and from patients with no upper gastrointestinal abnormality was studied in order to assess its effect on a formed fibrin clot. In both groups of patients gastric juice caused a marked increase in fibrinolysis as evidenced by a shortening of the euglobulin clot lysis time. This plasmin mediated fibrinolytic activity was found to be heat labile and only present in an acid environment. Addition of tranexamic acid or sucralfate to gastric juice almost completely reversed this effect, whereas pepstatin was only partially effective. It is probable that acid dependent proteases other than pepsin are responsible for the marked fibrinolysis. The ulcer healing agent sucralfate might be useful in those patients at risk of bleeding or rebleeding from active peptic ulcer disease.
PMCID: PMC1434462  PMID: 2612985
25.  Cigarette smoking, chronic peptic ulceration, and pepsin 1 secretion. 
Gut  1979;20(11):971-976.
The relationship between the secretion of pepsin 1 (the most electronegative of the pepsins), and the smoking habits of 219 patients has been investigated. Significantly more cigarette smokers with peptic ulceration (72.5%) secreted pepsin 1 in greater than trace amounts after pentagastrin or histamine than did non-smokers with ulceration (51.2%). Differences of a similar order were found for men with duodenal ulcer, women with duodenal ulcer, and all patients with gastric ulcer, but the difference was statistically significant only for men with duodenal ulcer. Significantly more patients with peptic ulcer smoking six to 15 cigarettes/day secreted moderate or high concentrations of pepsin 1 than did heavier smokers or non-smokers. There was no significant association between cigarette smoking and pepsin 1 secretion among 74 patients without ulceration. Maximal acid output was not significantly related to smoking in any group studied. The findings add to the increasing body of evidence linking pepsins and pepsin 1 with the pathogenesis of peptic ulceration.
PMCID: PMC1412681  PMID: 118897

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