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Background: Acrylamide input on gastric mucosa lesion is known but not fully elucidated. In this study the impact of dietary acrylamide on gastric acid secretion; an aggressive factor capable of causing erosion of the stomach tissue was evaluated to explain possible reason why acrylamide could induce gastric mucosa lesion. Thus, the study focuses on the impact of dietary acrylamide on gastric acid secretion and its association with mucosa lesion. Materials and Methods: Fifteen (15) male Sprague-Dawley rats were grouped into three groups (n = 5). Group 1 (control) was fed with standard rat diet, Group 2 and 3 were fed with standard rat diet contaminated with acrylamide doses (7.5mg/kg and 15mg/kg respectively) reported to compromise gastric mucosa integrity. The experimental animals were allowed free access to their various feed and drinking water ad libitum for 4 weeks. Impact of the dietary acrylamide on gastric acid secretion, gastric acidity and stomach tissue oxidative stress biomarkers (lipid peroxidation (MDA), superoxide dismutase (SOD), Glutathione peroxidase (GPx), and Catalase, CAT) were determined. Results: Average dietary consumption across the groups was 90.88% per week. Acrylamide contaminated diet significantly increased gastric acid secretion and gastric acidity in a dose dependent manner when compared to control, P<0.01. Dietary acrylamide also induced oxidative stress on stomach tissues by significantly increasing MDA as well as decreasing SOD, GPx, and CAT of the stomach in a dose dependent manner when compared to control, P<0.01. Conclusion: Findings from the study suggests that oxidative stress induced on stomach tissue by dietary acrylamide could be as a result of the increase in gastric acid secretion and gastric acidity observed.
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ABSTRACT Background and aim: It is well established that the rate of gastric lesions increases in diabetic rats. Recently, the protective effect of hydrogen sulfide (H2S) in gastric mucosa has been proven. This study aimed to determine the release of H2S and mRNA expression of cystathionine gamma lyase (CSE) in gastric mucosa in alloxan-diabetic rats in response to distention-induced gastric acid secretion. Twenty-four rats were randomly assigned to 4 groups (6 in each). They were the normal-control, distention-control, diabetic-control, and distention-diabetic groups. Under anesthesia, animals underwent a tracheotomy and midline laparotomy. To washout the gastric contents, a catheter was inserted in the stomach through the duodenum. To determine the effect of distention-induced gastric acid secretion on H2S release and mRNA expression of CSE, the stomachs were distended by normal saline. At the end of experiments, animals were sacrificed and the gastric mucosa was collected to determine H2S concentration and to quantify mRNA expression of CSE by quantitative real-time PCR. Mucosal release of H2S and mRNA expression of CSE significantly increased in response to stimulated gastric acid secretion in normal rats (P<0.01), while the increases in diabetic rats were not significant. Basal release of H2S and mRNA expression of CSE in gastric mucosa were significantly in diabetic rats lower than normal rats. On the basis of the results, we conclude that the decreased release of H2S in response to basal and stimulated gastric acid output in alloxan-diabetic rats compared to normal rats is largely due to downregulation of mRNA expression of CSE.
Subject(s)
Animals , Rats , Cystathionine gamma-Lyase , Gastric Acid , Hydrogen Sulfide , AlloxanABSTRACT
Objective:This study aimed to explore the Ventromedial Hypothalamic Orexin-1 and Orexin-1 Receptors in Regulation of Gastric Acid Secretion in Conscious Rats.Methods:Rats were anaesthetized and fitted with a stainless steel carmula placed just above the VMH or paracele,after random allocation orexin-A,[Pro34]-peptide YY and [CPP1-7,NPY19-23,Ala31,Aib32,Gln34] -pancreatic polypeptide were injected in the VMH;SB-334867 was intraperitoneal injection;atropine was subcutaneous injection;GR-231118 and CGP-71683 were injected in the paracele.Using pyloric ligation model,tests the effect of different drugs on rat gastric acid secretion and gastric juice volume.Results:OXA induced dose-dependent increase of gastric acid secretion;SB-334867 induced dose-dependent inhibition of gastric acid secretion.The stimulatory effect of OXA on acid secretion was inhibited by SB-334867;atropine induced dose-dependent increase of gastric acid secretion and block the effect of orexin-A on gastric acid secretion;the gastric acid secretion was inhibited by GR-231118 or CGP-71683,and GR-231118 or CGP-71683 were blocked the effect of orexin-A on gastric acid secretion;Intraventromedial hypothalamic injections of [CPP1-7,NPY19-23,Ala31,Aib32,Gln34]-pancreatic polypeptide increased gastric acid secretion.Conclusion:It is suggested that endogenous orexin-A acts on the ventromedial hypothalamus to stimulates acid secretion.This stimulatory effect is probably mediated through orexin receptor,Y1 and Y5 receptor,and the vagus nerve system.
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Aim of the study was to investigate Gastroprotective and anti-secretory effect of Pep-Up Tablet on pyloric ligation-induced gastric ulcer model in rats. Pep-Up Tablet is an Ayurvedic proprietary formulation which is manufactured and marketed by Vasu Healthcare Pvt. Ltd., Vadodara. The selected animals were divided into two groups and each group consisted of six animals. Group-I was considered as disease control and Group-II was as test drug (Pep-Up Tablet) treated group. Pep-Up Tablet (200 mg/kg/day, p.o.) was administered for 7 days by oral route in Group-II. Pep-Up Tablet was studied for its effect on ulcer index, gastric wall secretory parameters and mucin activity. Pretreatment of Pep-Up Tablet showed significant reduction in ulcer index, gastric acid secretion and pepsin activity. Pep-Up Tablet significantly increased mucin activity (TC:TP ratio) as well which was due to significant increase in the total carbohydrate content. From the available data of present study, it can be concluded that Pep-Up Tablet plays important role mainly on inhibition of acid secretion and in increase of mucin secretion which in turn enhances the stability of gastric mucosal barrier. Pep-Up Tablet provided significant gastric cytoprotection against pyloric ligation-induced gastric ulceration in rats.
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Aims: To evaluate the effects of the juice of Citrullus lanatus (watermelon) on gastric acid secretion and pH in Indomethacin-induced ulceration in male albino rats. Study Design: The experiment was divided into two studies. Under each study, four groups of rats were pre-treated with distilled water (control), 25% watermelon, 50% watermelon and 100% watermelon juice respectively for 30 days. Place and Duration of Study: Department of Physiology, College of Medicine, University of Ibadan, Ibadan, Nigeria, between June, 2011 and July, 2012. Methodology: Sixty-four animals in total were used for the experiment. The animals were divided into two experimental studies: Study I contained thirty-two rats which were used for the study on ulcerogenesis. Study II also contained thirty-two rats which were used for the study on gastric acid secretion. Each of the experimental studies was further divided into four groups in accordance with the study design. Results: Rats pre-treated with Citrullus lanatus juice exhibited significant dose-dependent reduction of gastric lesions formation (P<0.05). Also, ulcerogenesis in the pretreated groups was significantly lower than that observed with the control (P<0.05). Conclusion: The results suggest that Citrullus lanatus (watermelon) juice has a significant gastroprotective effect in Indomethacin-induced gastric ulceration. One of the mechanisms by which this protective effect is carried out is by its inhibition of gastric acid secretion.
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O uso dos inibidores da bomba protônica (IBPs) no tratamento da doença do refluxo gastroesofágico (DRGE) está bem estabelecido. Esta classe de medicamentos está indicada como primeira linha de tratamento para aliviar os sintomas e/ou cicatrizar as lesões esofágicas, sobretudo em pacientes com doença moderada a grave. Estudos randomizados e controlados têm demonstrado que os IBPs são mais eficazes que os antagonistas do receptores H2 no controle da supressão ácida do estômago. A secreção ácida nas células parietais do estômago cria um fluxo de íons, em que prótons são bombeados de fluidos intracelulares para o lúmen gástrico contra um gradiente. A engenharia enzimática responsável por este transporte ativo é a bomba H+,K+ ATPase, a qual é modulada (estimulação e inibição) por sinais moleculares neuronais e endócrinos. Os IBPs, após a ingestão antes da alimentação, ligam-se apenas às bombas ativadas. São metabolizados pelo complexo enzimático do citocromo P450, CYP 2C19 e CYP 3A4, esta característica contribui para interações medicamentosas com outros fármacos que também possuem o mesmo mecanismo de metabolização. Os IBPs, geralmente, são bem tolerados pelo organismo. Até o momento, estudos descreveram que as reações adversas mais comuns relatadas são dor de cabeça, diarreia e náusea, com incidência de < 10%, valores semelhantes quando comparados com placebo e antagonistas dos receptores H2. A terapia de supressão ácida com IBP está associada a benefícios no manejo de doenças ácido-pépticas. O sucesso desta supressão farmacológica para o processo de cicatrização de úlcera e DRGE está refletindo-se na redução de cirurgias eletivas como tratamento destas enfermidades, além da redução da gastropatia associada a utilização de AINEs...
Subject(s)
Stomach , Gastroesophageal RefluxABSTRACT
Objective To study the mechanism of Helicobacter Pylori inhibiting the healing of acetic acid - induced gastric ulcer in rats. Methods Rats were infected with Helicobacter Pylori and the model of acetic acid gastric ulcer was replicated at 4 weeks after in-fection. Amount of G cell and D cell in mucosa of gastric antrum, quantity of gastric juice and pH were measured at the 3rd,Sth, 16th day after the model was replicated. Results When the group of Hp + acetic acid ulcer compared with the group of acetic acid ulcer, the number of G cell, quantity of gastric juice increased (P < 0.01), and the number of D cell and pH decreased (P < 0.01). Conclusion Helicobacter Pylori inhibits ulcer healing through increasing gastric acid secretion.
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Os estudos sobre o efeito do controle do ácido gástrico iniciaram-se há mais de 30 anos. Desde então, inúmeros ensaios clínicos bem conduzidos e metanálises mostraram que os inibidores da bomba protônica (IBP) são significativamente mais efetivos que antagonistas dos receptores H2 da histamina para a realização da supressão ácida gástrica. A secreção ácida nas células parietais do estômago cria um fluxo de íons, em que prótons são bombeados de fluidos intracelulares para o lúmen gástrico contra um gradiente. A engenharia enzimática responsável por esse transporte ativo é a bomba H+,K+ ATPase, a qual é modulada (estimulação e inibição) por sinais moleculares neuronais e endócrinos. Os IBP, após a ingestão antes da alimentação, ligam-se apenas às bombas ativadas. São metabolizados pelo complexo enzimático do citocromo P450, CYP 2C19 e CYP 3A4, esta característica contribui para interações medicamentosas com outros fármacos que também possuem o mesmo mecanismo de metabolização. Os IBP, geralmente, são bem tolerados pelo organismo. Até o momento, estudos descreveram que as reações adversas mais comuns relatadas são: dor de cabeça, diarréia e náusea, com incidência de < 10%, valores semelhantes quando comparados com placebo e antagonistas dos receptores H2. A terapia de supressão ácida com IBP está associada a benefícios no manejo de doenças ácido-pépticas. O sucesso desta supressão farmacológica para o processo de cicatrização de úlcera e DRGE está refletindo-se na redução de cirurgias eletivas como tratamento destas enfermidades, além da redução da gastropatia associada à utilização de AINEs.
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Aim To study the effects of alumina, magnesia,and simethicone tabet on the secretion of gastric acid and pepsin activity in rats. Methods The pharmacodynamic indices were measured by the secretion of gastric acid and pepsin activity. Results and Conclusion Compared with the control group,alumina, magnesia, and simethicone inhibited gastric acid and increased pH of gastric juice.A significant decrease occurred in pepsin activity after a doses of 180 mg?kg-1 and 600 mg?kg-1 (P
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Objective Effects of Weiyanxiao on basal gastric- acid secretion in anesthetized rats were investigated.Methods pH value of gastric perfusate in rat models of gastric perfusion were detected with a precise acidity meter to evaluated the effects of Weiyanxiao on basal gastric- acid secretion and gastrin- induced acid secretion.Results Small- dose Weiyanxiao (12.3 g/kg) had no significant influence on basal gastric- acid secretion and has slight inhibition on high- level gastric- acid secretion induced by gastrin ;large- dose Weiyanxiao (24.6g/kg) could restrain basal gastric- acid secretion (P
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Famotidine ( Fam ) antagonized the effects of histamine on guinea pig atria and rat uteri MI vitro non-competitively,however the antagonisms of Ranitidine(Ran) and Cimetidine (Cim ) on hoistamine were competitive, their pA2 were 6. 24, 5. 16 and 4. 08 for guinea pig atria , 8. 26, 7. 22 and 6. 17 for rat uteri respectively. They reduced gastric secretion of acid and pepsin of pylorus ligated rats in dose-related manner, inhibited gastric secretion stimulated byhistamine, prevented the acute gastric lesion from stress, indomethacin and histamine, and enhanced the healing process of chronic gastirc ulcerinduced by acetic acid in rats. Moreover, Fam was much more potent than Ran (6~8 times) and Cim(30 - 40 times). Besides,Cim increased hypnotic effect of phenobartal, but Ran and Fam had no or Ittile such effects.
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The action of dl - tetrahydropal-matine(dl-THP) was studied in two preparations in vitro : the isolated rat gastric mucosa and parietal cells, dl-THP was found to inhibit significantly basal acid formation by the gastric mucosa in a dose - response fashion. The effect was reversible, acid secretion returning to control levels 1. 5~2h after the preparation underwent a double wash, dl - THP also produced asignificant and dose - dependent inhibition of histamine - induced secretion in the gastric mucosa and parietal cells, shifted the histamine dose -response cuver to the right and suppressed the maximum acid production, with pD_2~1 values of 4. 72 and 4. 70, respectively.
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To determine the effect of verapamil on experimental duodenal ulcer, pathologic assessment and secretory study were performed in the rats with ulcerogenic dose of cysteamine. The cysteamine increased gastric acid secretion and produced double duodenal ulcers at the proximal protion of the duodenum. Intramuscular injection of verapamil, 3 hours later, produced a significant decreased in gastric acid secretion which lasted at least 4 hours (cysteamine vs. cysteamine+ verapamil; 63.5 +/- 18.4 muEq vs. 25.5 +/- 9.0 muEq during the 1st hour after verapamil administration, 83.1 +/- 24.2 muEq vs. 27.8 +/- 12.3 muEq during the 2nd hour, 110.9 +/- 14.4 muEq vs. 38.5 +/- 25.9 muEq during the 3rd hour, 116.4 +/- 12.1 muEq vs. 40.7 +/- 29.6 muEq during the 4th hour, p less than 0.001). However, cysteamine-induced duodenal ulcers were not alleviated by two doses of intramuscular verapamil administration (4 mg/kg x 2). It is presumed that suppression of gastric acid secretion may not be sufficient to reduce cysteamine-induced duodenal ulcer formation or that verapamil itself may have aggresive effects against duodenum. To illucidate the exact role of verapamil in cysteamine-induced duodenal ulcer, further studies would be needed.
Subject(s)
Animals , Male , Rats , Cysteamine , Duodenal Ulcer/chemically induced , Gastric Acid/metabolism , Injections, Intramuscular , Rats, Inbred Strains , Stomach/drug effects , Verapamil/therapeutic useABSTRACT
Ethanol causes mucosal injury to the stomach and which accompanied by back-diffusion of H+. Using several drugs known to modify the gastric acid secretion and to provide cytoprotection the effect of back-diffusion of H+ by ethanol was examined. Following 48 hours of starvation rats were anesthetized with urethane, and their stomachs were filled with 4 ml of 20% ethanol solution containing 1.8 mM HCI (7.2 microEq/4 ml) every 15 min. H+ content of the collected perfusates was determined by back-titration to pH 6.0. The presence of ethanol in the stomach for 1 hour caused a loss of luminal H+ at a rate of 4.8 +/- 0.4 microEq/15 min. Pretreatment of rats with atropine (2 mg/Kg, i.v.), pirenzepine(2 mg/Kg. i.v.), cimetidine (10mg/Kg i.v.), cromolyn sodium (20mg/Kg/hr, i.v.) or domperidone (1 mg/kg. i.v.) did not affect the ethanol-induced H+ back-diffusion. Similarly, no effect was seen in rats treated with prostaglandin E2 (100 microgram/Kg i.v.) or indomethacin (5 mg/Kg, s.c). The addition of procaine (10(-5)~10(-3) M) or propranolol (10(-9)~10(-5) M) to the perfusate did not cause any changes in the ethanolinduced H+ back-diffusion. However, pretreatment of rats with acetazolamide (100 mg/Kg i.v.) or ethoxzolamide(50 mg/Kg/day, p.o. for 6 days), carbonic anhydrase inhibitors, markedly suppressed the ethanol-induced loss of luminal H+. Based on these results, it is suggested that ethanol-induced back-diffusion of H+ is mediated, at least in part, by the activity of carbonic anhydrase, and that cholinergic, histaminergic and dopaminergic mechanisms are not involved. Moreover, the implications of prostaglandins and membrane stability are not suggested.