Duodenal Ulcers In Rats Research Articles

Evaluation of Antiulcer Potential of <i>Bougainvillea spectabilis</i> Extracts on Cysteamine Hydrochloride-Induced Duodenal Ulceration in Rats

Evaluation of Antiulcer Potential of <i>Bougainvillea spectabilis</i> Extracts on Cysteamine Hydrochloride-Induced Duodenal Ulceration in Rats

From Selye's and Szabo's Cysteamine-Duodenal Ulcer in Rats to Dopamine in the Stomach: Therapy Significance and Possibilities.

We reviewed gastric ulcer healing by dopamine considering several distinctive duodenal key points. Selye and Szabo describe the cysteamine-induced duodenal ulcer in rats as a duodenal stress ulcer in patients. Szabo's cysteamine duodenal ulcer as the dopamine duodenal healing and cysteamine as a dopamine antagonist signifies the dopamine agonists anti-ulcer effect and dopamine antagonists ulcerogenic effect. From these viewpoints, we focused on dopamine and gastric ulcer healing. We mentioned antecedent studies on the dopamine presence in the stomach and gastric juice. Then we reviewed, in the timeline, therapy significance arising from the anti-ulcer potency of the various dopamine agonists, which is highly prevailing over the quite persistent beneficial evidence arising from the various dopamine antagonists. Meanwhile, the beneficial effects of several peptides (i.e., amylin, cholecystokinin, leptin, and stable gastric pentadecapeptide BPC 157, suggested as an acting mediator of the dopamine brain-gut axis) were included in the dopamine gastric ulcer story. We attempt to resolve dopamine agonists/antagonists issue with the dopamine significance in the stress (cysteamine as a prototype of the duodenal stress ulcer), and cytoprotection (cysteamine in small dose as a prototype of the cytoprotective agents; cysteamine duodenal ulcer in gastrectomized rats). Thereby, along with dopamine agonists' beneficial effects, in special circumstances, dopamine antagonists having their own ulcerogenic effect may act as "mild stress (or)" or "small irritant" counteracting subsequent strong alcohol or stress procedure-induced severe lesions in this particular tissue. Finally, in the conclusion, as a new improvement in further therapy, we emphasized the advantages of the dopamine agents' application in lower gastrointestinal tract therapy.

Traditional Chinese Medicine prescription Huang-Qi-Jian-Zhong-Tang ameliorates indomethacin-induced duodenal ulcers in rats by affecting NF-κB and STAT signaling pathways

Huang-Qi-Jian-Zhong-Tang (HQJZT) is a well-known traditional Chinese herbal formulation. This study aimed to investigate the duodenoprotective properties of HQJZT against Indomethacin (IND)-induced duodenal ulceration in rats, and the mechanisms involved, particularly through NF-κB and STAT signaling pathways. Our results showed that HQJZT completely protected the duodenal mucosa from ulceration caused by IND, as indicated by improved macroscopic and histological appearances. There was a significant decrease in ulcer index and microscopic score, an increase in villus height and crypt depth, and a normalization of the tissue architecture of the duodenum in rats following HQJZT treatment. Blood flow into the duodenal mucosa was significantly increased after HQJZT administration. HQJZT significantly increased PGE2 and NO levels in the duodenal mucosa. A significant reduction in the production of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α was observed in the duodenal mucosa under treatment with HQJZT. Mechanistically, the administration of HQJZT significantly lowered the duodenal protein expression of inflammation-related genes, including p-NF-κB and p-IκBβ, compared with the ulcer control group. Furthermore, the STAT signaling pathway-related protein markers p-JAK and p-STAT were significantly reduced in the HQJZT (1.30 and 2.60 g/kg) groups. As a result of these findings, HQJZT alleviates duodenal mucosal ulcers caused by IND. A protective effect of HQJZT on duodenal ulcers is attributed to its ability to improve mucosal blood flow, stimulate the production of cytoprotective mediators, minimize proinflammatory cytokines, and block the activation of NF-κB and STAT signaling pathways.

Protective effect and mechanisms of action of Mongolian medicine Sulongga-4 on pyloric ligation-induced gastroduodenal ulcer in rats.

BACKGROUNDSulongga-4 (SL-4) is a herbal formula used in traditional Mongolian medical clinics for the treatment of peptic ulcers and gastroenteritis, even though its pharmacological mechanism has not been well characterized.AIMTo evaluate the protective effect and identify the mechanisms of action of SL-4 on gastroduodenal ulcer induced by pyloric ligation (PL) in rats.METHODSPL was performed to induce gastric and duodenal ulcers in rats, which were then treated with oral SL-4 (1.3, 2.6, or 3.9 g/kg per day) for 15 d. PL-induced gastroduodenal ulceration. Therapeutic effects were characterized by pathological and histological evaluations and inflammatory indicators were analyzed by enzyme-linked immunosorbent assay. Microarray analyses were conducted to identify gene expression profiles of gastroduodenal tissue in PL rats with or without SL-4 treatment. The candidate target genes were selected and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR).RESULTSSL-4 decreased histopathological features in the PL-induced ulcerated rats. SL-4 significantly (P < 0.05) decreased expression of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, endotoxin, platelet-activating factor, and increased prostaglandin E2 and epidermal growth factor in ulcer tissue. Microarray analysis was used to identify a panel of candidate target genes for SL-4 acting on PL-induced ulceration. Genes included some complement and coagulation cascade and retinol metabolism pathways that are closely associated with inflammatory responses and gastric mucosal protective mechanisms. qRT-PCR showed that altered expression of the selected genes, such as CYP2b2, UGT2b1, A2m, and MASP1 was consistent with the microarray results.CONCLUSIONSL-4 exerts protective effects against PL-induced gastroduodenal ulcers via reducing inflammatory cytokines and elevating expression of gastric acid inhibitory factors. Downregulation of CYP2b2 and UGT2b1 genes in retinol metabolism and upregulation of A2m and MASP1 genes in the complement and coagulation cascades pathways are possibly involved in SL-4-mediated protection against gastroduodenal ulcer.

Antiulcerogenic Activity of Li-Zhong Decoction on Duodenal Ulcers Induced by Indomethacin in Rats: Involvement of TLR-2/MyD88 Signaling Pathway.

Background Administration of nonsteroidal anti-inflammatory drugs (NSAIDs) often causes small intestinal ulcers in patients, but few effective drugs are currently available to manage such serious adverse events of NSAIDs. Li-Zhong decoction (LZD), a well-known traditional Chinese medicine (TCM) formula, is commonly prescribed for treatment of gastrointestinal diseases. The present study aimed to investigate the anti-ulcerogenic activity of LZD on indomethacin- (IND-) induced duodenal ulcer in rats. Mechanistic studies of action of LZD were focused on involvement of TLR-2/MyD88 signaling pathway. Methods Fifty male Sprague-Dawley (SD) rats were randomly and evenly divided into five groups: normal control, ulcer control (IND, 25 mg/kg), IND + esomeprazole (ESO, 4.17 mg/kg), and IND + low and high doses of LZD (3.75 and 7.50 g/kg). Macroscopic and histopathological examinations were performed for evaluation of ulcer index (UI), curative index (CI), and microscopic score (MS). Levels of duodenal inflammatory biomarkers and cytoprotective mediators including interleukin-4 (IL-4), IL-10, tumor necrosis factor-α (TNF-α (TNF-Results Gross and microscopic examinations of the IND-treated rats revealed severe duodenal hemorrhagic necrosis, inflammatory infiltration, villus destruction, and crypt abscess, while LZD-treated rats manifested these pathological events to a markedly lesser degree. LZD significantly decreased UI and MS, increased CI, preserved the integrity of the villus and crypt, and normalized the tissue architecture of the duodenum of rats. The elevated TNF-α (TNF-Conclusions Our data demonstrate that LZD protects the duodenal mucosa from IND-caused lesions, which is at least partially attributable to the interaction of its potential cytoprotective and anti-inflammatory mechanisms together with enhancement of the mucosal immunity through TLR-2/MyD88 signaling pathway.

Prevalence of Helicobacter pylori and its CagA subtypes in gastric cancer and duodenal ulcer at an Austrian tertiary referral center over 25 years.

Background and aimsThe prevalence of Helicobacter pylori (H. pylori) tends to be lower in Western countries such as central Europe compared with Asia. The virulence of H. pylori is influenced by its subtype composition, most importantly by the presence or absence of different types of cytotoxin-associated gene A(CagA). This study aimed to assess the prevalence of H. pylori and its respective CagA phenotype in a large retrospective cohort of patients with gastric cancer or duodenal ulcer at a Western tertiary referral institution.MethodsH. pylori positive gastric biopsy samples from patients diagnosed with the afore mentioned diseases within the past 25 years were re-evaluated by histology for H. pylori and status of gastritis. Confirmed H. pylori positive cases were processed for immunohistochemistry (IHC) for H. pylori,CagA, and EastAsiantype CagA.ResultsThe prevalence of H. pylori positive gastric biopsy samples decreased from 20.7% to 2.3% within the study period. Among the gastric cancer patients, the H. pylori positive rate was 16.6%, and didn’t show significant changes over time (p = 0.38). Contrary, the H. pylori positive rate of duodenal ulcer decreased significantlyfrom 40% to 5% (p = 0.01). Within H. pylori positive groups ofboth diseases, CagA was highly detected at IHC (86% and 78%, respectively). Except for a few patients originating from East Asian countries, all CagA detected in this study were of Western type.ConclusionIn this first Western investigation on the chronological prevalence of H. pylori and its most relevant subtypes, Western type of CagA was highly detected in two important index diseases of the pathogen. This raises further questions about the virulence of this subtype.

Anti-ulcerative, Anti-oxidative, and Anti-inflammatory Effects of Rosuvastatin and Isosorbide Dinitrate on Cysteamine-Induced Chronic Duodenal Ulcer in Rats

Background: Methotrexate (MXT) is the corner stone in treatment of rheumatoid arthritis. Although methotrexate is usually administrated in low weakly dose in patients with rheumatoid arthritis discontinuation rates are as high as 16% due to adverse effects. Hepatotoxicity is the most common side effect after long term course of methotrexate. Aim of the study: This work aimed to investigate the potential effect of sitagliptin alone and in combination with different doses of methotrexate on rheumatoid arthritis (RA) induced experimentally in rats. Moreover, we investigated the benefits of sitaglipitn co-administration with methotrexate not only on RA progression, but also on organs commonly injured on using methotrexate alone as a disease-modifying anti-rheumatic drug such as the liver. Methods: 42 male adult Sprague Dawley rats divided into seven equal groups: Normal control group, None treated Freund,s adjuvant induced rheumatoid arthritis,High dose MXT treated rheumatoid arthritis (1 mg/kg/3 days i.p.) over 4 weeks,Sitagliptin treated rheumatoid arthritis (10 mg/kg/day p.o) for 4 weeks, high dose MXT+ sitagliptin treated arthritis, 1/2 dose MXT+ sitagliptin treated arthritis, 1/4 dose MXT+ sitagliptin treated arthritis. Serological parameters namely, cyclic citrullinated peptide antibodies (Anti-CCP), matrix metalloproteinase-3(MMP-3), cartilage oligometric matrix protein (COMP) and TNF-α level were measured. Liver tissue and hind paw joint were subjected to histopathological examination. Results: Best degree of improvement was obtained with high dose MXT+ sitagliptin. It is significantly better than that of either drug alone. Half dose of MXT /sitagliptin combination was proved to be equally effective to the full dose of methotrexate alone regarding all tested parameters. Conclusion: concomitant administration of sitagliptin augmented immunosuppressive effect and ameliorated hepatotoxicity of methotrexate in Freund,s adjuvant model of rheumatoid arthritis.

Anti-ulcerative, Anti-oxidative, and Anti-inflammatory Effects of Rosuvastatin and Isosorbide Dinitrate on Cysteamine-Induced Chronic Duodenal Ulcer in Rats

Anti-ulcerative, Anti-oxidative, and Anti-inflammatory Effects of Rosuvastatin and Isosorbide Dinitrate on Cysteamine-Induced Chronic Duodenal Ulcer in Rats

Efficacy of proton pump inhibitors for patients with duodenal ulcers: A pairwise and network meta-analysis of randomized controlled trials

Background/Aim:To compare the efficacy and tolerance of different proton pump inhibitors (PPIs) in different doses for patients with duodenal ulcers.Materials and Methods:An electronic database was searched to collect all randomized clinical trials (RCTs), and a pairwise and network meta-analysis were performed.Results:A total of 24 RCTs involving 6188 patients were included. The network meta-analysis showed that there were no significant differences for the 4-week healing rate of duodenal ulcer treated with different PPI regimens except pantoprazle 40 mg/d versus lansoprazole 15 mg/d [Relative risk (RR) = 3.57; 95% confidence interval (CI) = 1.36–10.31)] and lansoprazole 30 mg/d versus lansoprazole 15 mg/d (RR = 2.45; 95% CI = 1.01–6.14). In comparison with H2 receptor antagonists (H2 RA), pantoprazole 40 mg/d and lansoprazole 30 mg/d significantly increase the healing rate (RR = 2.96; 95% CI = 1.78–5.14 and RR = 2.04; 95% CI = 1.13–3.53, respectively). There was no significant difference for the rate of adverse events between different regimens, including H2 RA for a duration of 4-week of follow up.Conclusion:There was no significant difference for the efficacy and tolerance between the ordinary doses of different PPIs with the exception of lansoprazle 15 mg/d.

MPTP-induced duodenal ulcers in rat. Prevention by reuptake blockers for serotonin and norepinephrine, but not dopamine.

Abnormal activity of dopamine, serotonin, and norepinephrine may contribute to the pathophysiology of duodenal ulcers. We therefore studied the effects of neuropharmacological manipulations on 1-methly-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP)-induced duodenal ulcers. Duodenal ulcers were produced in rats by 12 subcutaneous injections of a neurotoxin, MPTP, over 4 days. At an MPTP dose of 20 mg.kg. injection, duodenal ulcers developed in 91% (43 of 47) of animals with low mortality. When neuropharmacological agents were preadministered before MPTP, the following effects on duodenal ulcers incidence were obtained. MAO-B inhibitors (pargyline [55%], deprenyl [43%]) but not MAO-A inhibitors (clorgyline [91%]) significantly decreased the frequency of duodenal ulcers suggesting that, like MPTP-induced parkinsonism, formation of a toxic metabolite, probably 1-methyl-4-phenyl-pyridinium is involved. Reuptake blockers for serotonin (fluoxetine [18%], indalpine [25%]) also decreased the frequency of duodenal ulcers. Reuptake blockers for norepinephrine (desmethylimipramine [17%], tomoxepine [31%], but not amfonelic acid [82%]) decreased the frequency of duodenal ulcers. Reuptake blockers for dopamine (benztropine [73%], amfonelic acid [82%], GBR-12909 [80%]) did not protect against duodenal ulcers. However, GBR-12909 significantly decreased the severity of those duodenal ulcers that were produced. These data suggest that abnormally low levels of synaptic transmission in serotonergic and possibly noradrenergic neurons play an important role in the pathogenesis of duodenal ulcer while the role of dopamine may be limited to modulation of ulcer severity.

Evaluation of the antiulcer potential of Punica granatum (pomegranate) peel extract on indomethacin-induced duodenal ulcer

Introduction: Duodenal ulcer is a serious public health problem that affects approximately 10% of the global population and is two to three times more prevalent than gastric ulcer. Naturally occurring medications for duodenal ulcer include the use of pomegranate rind powder. This traditional medication has been used in Saudi Arabia for many years. Objectives: To investigate the capacity of pomegranate peel extract in healing and preventing duodenal ulceration in rats. Materials and methods: Experimental animals were divided into four groups. Group I was used as a control. In Group II (ulcer group) duodenal ulcer was induced by indomethacin administration using a single oral dose of 25mg/kg. In Group III (prevention group), 2 weeks before ulcer induction, rats were treated orally with pomegranate peel extract or ranitidine. In Group IV (treatment group), after ulcer induction, rats were treated with pomegranate peel extract or ranitidine for 2 weeks. The duodenum was subjected to light microscopic studies, immunohistochemical detection of Ki67 as a proliferative marker and biochemical studies (measuring the parameter of lipid peroxidation). Statistical analyses were carried out for determination of the significance of changes in Ki67 proliferation index. Results: In the ulcer group, the levels of malondialdehyde were significantly increased while the reduced glutathione activity was lowered in duodenal mucosa compared with the control group. Apparent disturbed villous to crypt ratio with necrosis and cellular lysis at the tip of the villi and marked mononuclear cellular infiltration were observed in the ulcer group. There was preservation of the crypt to villous ratio, an increase in goblet cells and decreased levels of malondialdehyde in the protection and treatment groups. The number of Ki67 immunostained cells was also increased in these groups. Conclusions: The use of pomegranate rind powder gave good results in the treatment, and perhaps also prevention, of duodenal ulceration in rats.

A study on healing of peptic ulcer disease after eradication of helicobacter pylori infection

There is intimate connection between peptic ulcer &amp; Helicobacter pylori infection. But some uncertainties still surround the relationship between status of H. pylori infection and extent &amp; time required for ulcer healing. This prospective observational study was carried out in the department of Gastroenterology, BSMMU, Dhaka from January 2007 to January 2008 to determine whether the successful eradication of H. pylori leads to adequate ulcer healing. To see the pattern of endoscopic findings in patients still having H. pylori infection after standard triple therapy for H. pylori were also a objective. Eighty nine consecutive patients, aged 15-60 years and of both genders, coming to the gastroenterology outpatient department with the symptoms suggestive of peptic ulcer disease and dyspepsia were included and H. pylori status was defined as positive if both rapid urease test &amp; histopathology were positive. As found in this study, H. pylori was associated with 90% of duodenal ulcers and 80% of gastric ulcers. H. pylori eradication rate was 69%. Healing rate of duodenal ulcer and gastric ulcer after standard triple therapy for 14 days were 80% and 78% respectively. Adequate ulcer healing was achieved in this study despite relatively low eradication rate. Follow-up for additional period is required for recurrence of ulcer in 84 patients whose peptic ulcer disease had resolved but could not attain H. pylori eradication and H. pylori eradicated patients who are still having ulcer at endoscopy DOI: http://dx.doi.org/10.3329/bmj.v43i2.21388 Bangladesh Med J. 2014 May; 43 (2): 84-89

STAT3 and Importins Are Novel Mediators of Early Molecular and Cellular Responses in Experimental Duodenal Ulceration

Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that directly upregulates VEGF, Ref-1, p21, and anti-apoptotic genes such as Bcl-xL. In this study, we hypothesized that STAT3 signaling is activated and provides a critical protective role that is required for enterocyte survival during the early phases of cysteamine-induced duodenal ulcers. We studied the effect of inhibition of STAT3 activity on cysteamine-induced duodenal ulcers in rats and egr-1 knockout mice using STAT3/DNA binding assay, immunohistochemistry, immunoblot, and quantitative reverse transcriptase PCR analyses. We found that G-quartet oligodeoxynucleotides T40214, a specific inhibitor of STAT3/DNA binding, aggravated cysteamine-induced duodenal ulcers in rats 2.8-fold (p<0.05). In the pre-ulcerogenic stage, cysteamine induced STAT3 tyrosine phosphorylation, its translocation to nuclei, an increased expression and nuclear translocation of importin α and β in the rat duodenal mucosa. Cysteamine enhanced the binding of STAT3 to its DNA consensus sequences at 6, 12, and 24h after cysteamine by 1.5-, 1.8-, and 3.5-fold, respectively, and activated the expression of STAT3 target genes such as VEGF, Bcl-xL, Ref-1, and STAT3-induced feedback inhibitor, a suppressor of cytokine signaling 3. We also demonstrated that egr-1 knockout mice, which are more susceptible to cysteamine-induced duodenal ulcers, had lower levels of STAT3 expression, its phosphorylation, expression of importin α or β, and STAT3/DNA binding than wild-type mice in response to cysteamine. Thus, STAT3 represents an important new molecular mechanism in experimental duodenal ulceration.

Antiulcer Activity of Patol Churna against Experimental Gastro-duodenal Ulcers in Rats

Patol churna is a well known ayurvedic formulation of Trichosanthes cucumerina Linn. (cucurbitaceae) administered in case of number of alimentary and liver disorders. It is widely used in Indian folk medicine for variety of disease conditions. The aim of present study was to evaluate the antiulcer activity of 50% ethanolic extract of patol churna (PCE) using various experimental models of gastric and duodenal ulceration in rats. Oral administration of 50% ethanolic extract of patol churna was evaluated in rats against ethanol, aspirin and pylorus ligated gastric ulcers as well as cysteamine-induced duodenal ulcers. In all the models studied, the antiulcer activity of PCE compared with that of cimetidine (100mg/kg, p.o.), an H 2 receptor antagonist. PCE showed significant antiulcer activity in ethanol-induced and aspirin-induced gastric ulcer models. In 19 hrs pylorus ligated rats, significant reduction in ulcer index, total acidity and pepsin activity was observed with PCE, when compared with the control group. Mucosal defensive factors such as pH, mucin activity and gastric wall mucous content was found to be increased with PCE. PCE was also, afforded remarkable protection in cysteamine-induced duodenal lesions. The antiulcer activity of PCE was comparable with that of cimetidine. Thus, patol churna extract possess significant antiulcer activity against both gastric and duodenal ulcers in rats. The antiulcer activity may be attributed to its cytoprotective action and inhibition of acid secretary parameters

Ghrelin accelerates the healing of cysteamine-induced duodenal ulcers in rats

SummaryBackgroundPrevious studies have shown that administration of ghrelin exhibits protective and therapeutic effects in the gut. The aim of the present investigation was to examine the influence of ghrelin administration on the course of cysteamine-induced duodenal ulcers, as well as effects on mucosal production of oxygen free radicals and duodenal antioxidant defense.Material/MethodsDuodenal ulcers were induced in male Wistar rats by cysteamine administered intragastrically at the dose of 200 mg/kg in 1 ml of saline, 3 times at 4-h intervals. Starting 24 h after the first dose of cysteamine, rats were treated intraperitoneally twice a day with saline or ghrelin given at the dose of 4, 8 or 16 nmol/kg/dose. Seven days after administration of the first dose of cysteamine, the study was terminated.ResultsInduction of ulcers by cysteamine was accompanied by a reduction in duodenal blood flow, mucosal DNA synthesis and mucosal activity of superoxide dismutase (SOD); whereas mucosal concentration of interleukin-1β and malonyldialdehyde (MDA – an index of lipid peroxidation) were increased. Treatment with ghrelin increased healing rate of duodenal ulcers and enhanced duodenal blood flow, mucosal DNA synthesis and mucosal activity of SOD, and reduced mucosal concentration of interleukin-1β and MDA.ConclusionsTreatment with ghrelin increases the healing rate of duodenal ulcers and this effect is related, at least in part, to improvement of duodenal mucosal blood flow, mucosal cell proliferation and antioxidant defense, as well as being related to reduction in mucosal oxidative stress and inflammatory response.

Cytoprotective Effect ofMorinda tinctoriaRoxb. against Surgical and Chemical Factor Induced Gastric and Duodenal Ulcers in Rats

The present paper relates to the pharmacological validation of the antiulcer efficacy of ethanol leaf extract ofMorinda tinctoriaRoxb. (EEMT) against aspirin pyloric ligation-induced gastric ulcer model and cysteamine-induced duodenal ulcer in Wistar rats. Oral administration of EEMT at a dose of 200 and 400 mg/kg significantly prevented the occurrence of aspirin pyloric ligation and cysteamine-induced gastric and duodenal ulceration. The volume and acidity of gastric juice in pyloric ligated rats were significantly () reduced by EEMT. There was a significant decrease in the number of ulcers, and its severity in both the models proved the ulcer protective activity of EEMT. Administration of extract at both dose levels has shown a significant increase in potassium and sodium ion concentration in the gastric juice of pylorus ligation group. On the basis of these observations, we concluded that EEMT possessing antiulcer activity may be due to the modulation of defensive factors by improvement in gastric cytoprotection.

Gastric antisecretory and anti-ulcer effect of ME3407, a new benzimidazole derivative, in rats.

The effects of a new benzimidazole derivative, ME3407 (n-butyl-2-(thiazolo-[5,4-b]pyrid-2-yl) sulfinylacetate, CAS 133903-90-9), on gastric acid secretion and gastric and duodenal ulcers in rats were examined. ME3407, given orally, inhibited dose-dependently (0.3-30 mg/kg) the incidence of gastric lesions such as Shay ulcers, and water-immersion stress-, acetylsalicylic acid (ASA)- and histamine-induced erosions. In addition, ME3407 showed marked therapeutic effect on HCl- and ASA-induced lesions. In the lumen-perfused rats, oral administration of ME3407 inhibited dose-dependently (1-100 mg/kg) gastric acid secretion induced by histamine and tetragastrin with ED50 values of 3.02 and 3.37 mg/kg, respectively. Oral administration of ME3407 at a dose of 30 mg/kg also inhibited the elevation of serum gastrin level. The development of duodenal ulcers caused by mepirizole and systeamine was also potently inhibited by ME3407 at an oral dose of 0.1-30 mg/kg. However, when given at 30 mg/kg intraduodenally, subcutaneously or intravenously, ME3407 did not inhibit these acutely induced gastric elosion and acid output. ME3407 was not detected in the serum upon oral administration. These results indicated that ME3407 was active only by oral administration, and exerts direct action on the ulcers and acid secretion from the gastric membrane.

Effect of andrographolide on cysteamine-induced duodenal ulcer in rats

The aim of this study was to evaluate the gastroprotective efficacy of andrographolide isolated from Andrographis paniculata in rats induced with duodenal ulcers. Duodenal ulcers were induced by cysteamine administration in rats pretreated with 3 mg kg−1 BW day−1 of andrographolide for 30 days. Ulcer score, myeloperoxidase activity, TBARS level, GSH/GSSG ratio and enzyme antioxidants were measured in the duodenal tissue. Brush border and basolateral membranes were isolated to assay sucrase, maltase, alkaline phosphatase and total ATPases. Ulcer score was significantly minimised in rats pretreated with andrographolide. Elevation in myeloperoxidase and TBARS levels were found to be minimised significantly due to andrographolide treatment. Membrane-bound enzyme activities and the thiol redox status of glutathione were significantly maintained in duodenal mucosa of rats that received andrographolide. This study reveals that the major component of A. paniculata, andrographolide, has potent antiulcer properties that are most likely caused by minimising inflammatory changes, counteracting free radical formation and maintaining the thiol redox status in the duodenum.

Effect of lapachol, a naphthaquinone isolated from Tectona grandis, on experimental peptic ulcer and gastric secretion

Lapachol, a naphthaquinone isolated from the roots of Tectona grandis given at a dose of 5 mg kg-1 p.o. twice daily for 3 days was found to have an anti-ulcerogenic effect on subsequently induced experimental gastric and duodenal ulcers in rats and guinea-pigs. Its action appears to be associated with an effect on the protein content of gastric juice, and it reversed aspirin-induced changes in peptic activity, protein and sialic acid.

Pharmacological efficacy of argemone mexicana plant extract, against cysteamine-induced duodenal ulceration in rats

The plant Argemone mexicana is traditionally used as diuretic, anti-inflammatory, antibacterial, antifungal agent, and has wound-healing property. This study was carried out to evaluate the effect of A. mexicana aerial part of the plant (methanolic and aqueous extract p.o.) on duodenal ulceration. The study was carried out on the duodenal ulceration model by using cysteamine hydrochloride. Ranitidine (20 mg/kg) was used as standard drug. Both the extracts of the plant A. mexicana produced a significant activity in cysteamine-induced duodenal ulceration. The aqueous extract at the dose-dependent manner showed the potent activity than methanolic extract. The plant A. mexicana Linn. Increased healing of gastric ulceration and prevented the development of experimentally induced duodenal ulceration in rats.