Relevant bibliographies by topics / Gastric mucosa Effect of drugs on

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Academic literature on the topic 'Gastric mucosa Effect of drugs on'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 January 2023

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Journal articles on the topic "Gastric mucosa Effect of drugs on"

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Lavy, Alexandra. "Corrosive Effect of Nifedipine in the Upper Gastrointestinal Tract." Diagnostic and Therapeutic Endoscopy 6, no. 1 (January 1, 1999): 39–41. http://dx.doi.org/10.1155/dte.6.39.

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Upper gastrointestinal tract mucosa is prone to injury. Drugs may disturb gastric mucosa protective mechanisms and cause damage. Injury by NSAIDs is a well described complication. Nifedipine, a widely used drug, was not described before as having a potential to damage gastrointestinal mucosa. We describe here, two patients, who developed esophageal and gastric mucosal damage, probably related to Nifedipine ingestion.
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Lu, Sheng-Yu, Song Guo, Shao-Bin Chai, Jia-Qi Yang, Yuan Yue, Hao Li, Pei-Ming Sun, et al. "Autophagy in Gastric Mucosa: The Dual Role and Potential Therapeutic Target." BioMed Research International 2021 (June 11, 2021): 1–8. http://dx.doi.org/10.1155/2021/2648065.

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The incidence of stomach diseases is very high, which has a significant impact on human health. Damaged gastric mucosa is more vulnerable to injury, leading to bleeding and perforation, which eventually aggravates the primary disease. Therefore, the protection of gastric mucosa is crucial. However, existing drugs that protect gastric mucosa can cause nonnegligible side effects, such as hepatic inflammation, nephritis, hypoacidity, impotence, osteoporotic bone fracture, and hypergastrinemia. Autophagy, as a major intracellular lysosome-dependent degradation process, plays a key role in maintaining intracellular homeostasis and resisting environmental pressure, which may be a potential therapeutic target for protecting gastric mucosa. Recent studies have demonstrated that autophagy played a dual role when gastric mucosa exposed to biological and chemical factors. More indepth studies are needed on the protective effect of autophagy in gastric mucosa. In this review, we focus on the mechanisms and the dual role of various biological and chemical factors regulating autophagy, such as Helicobacter pylori, virus, and nonsteroidal anti-inflammatory drugs. And we summarize the pathophysiological properties and pharmacological strategies for the protection of gastric mucosa through autophagy.
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Andrews, F. J., C. Malcontenti-Wilson, and P. E. O'Brien. "Effect of nonsteroidal anti-inflammatory drugs on LFA-1 and ICAM-1 expression in gastric mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 4 (April 1, 1994): G657—G664. http://dx.doi.org/10.1152/ajpgi.1994.266.4.g657.

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Leukocyte adhesion to the endothelium appears to play an important role in gastric injury. This study aimed to develop immunohistochemical staining techniques to investigate the distribution and sequence of expression of both leukocyte [lymphocyte function associated antigen 1 (LFA-1)] and endothelial [intracellular adhesion molecule 1 (ICAM-1)] adhesion molecules in the mucosa after treatment with nonsteroidal anti-inflammatory drugs (NSAIDs). In control rats there were 803 +/- 72 LFA-1-stained cells/mm2 in the deep mucosa, 134 +/- 32 cells/mm2 in the superficial mucosa, and 6.4 +/- 1.2 ICAM-1-stained blood vessels/mm2 in the total mucosa. The number of ICAM-1-stained blood vessels in the mucosa increased significantly after 30 min of treatment with intragastric aspirin (30 mM; 25.2 +/- 7.2/mm2, P < 0.01) and indomethacin (20 mg/kg; 20.7 +/- 4.4/mm2, P < 0.01) before any appreciable mucosal damage was evident. This increase was reversed by treatment with misoprostol (100 micrograms/kg) in both aspirin- (7.6 +/- 1.7/mm2, P < 0.01) and indomethacin-treated animals (10.7 +/- 2.6/mm2, P < 0.05). There was no significant increase in LFA-1-positive cells until 60 min of NSAID treatment. We conclude that the adhesion molecules LFA-1 and ICAM-1 are expressed in the normal gastric mucosa and that the number of ICAM-1-stained blood vessels increase rapidly after NSAID treatment. This increase in ICAM-1 expression may be associated with an inhibition of prostaglandin synthesis by NSAIDs. These results provide further support for the role of early vascular changes in NSAID gastropathy.
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Fang, Yan Fei, Wen Li Xu, Lan Wang, Qing Wu Lian, Li Feng Qiu, Hui Zhou, and Shu Jie Chen. "Effect of Hydrotalcite on Indometacin-Induced Gastric Injury in Rats." BioMed Research International 2019 (April 11, 2019): 1–9. http://dx.doi.org/10.1155/2019/4605748.

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Background and Aims. Hydrotalcite plays an important role in the therapy of gastric ulcer induced by nonsteroidal anti-inflammatory drugs (NSAIDs), but little is known about the mechanism. We designed two experiments to study the preventive and curative effects of hydrotalcite on NSAIDs-related gastric injury in rats and to investigate the relationship between the protective and curative mechanism of hydrotalcite and the secretion of epidermal growth factor (EGF)/prostaglandin E2 (PGE2). Methods. Two experiments were separately designed to evaluate the preventive and curative effects of hydrotalcite. A total of 25 male rats and 25 female rats were randomly divided into five groups (vehicle group, model group, omeprazole group, hydrotalcite group, and ranitidine group) in each experiment. Rats were treated with indomethacin by gavage to build the model of acute gastric mucosal injury. The concentrations of EGF and PGE2 in blood specimens and mucosal injury indexes by gross inspection were measured and an immunohistochemical technique was also employed to test the levels of EGF, cyclooxygenase-1 (COX-1), and cyclooxygenase-2 (COX-2) in gastric mucosa. Results. Comparing with model group in both preventive and curative experiments, hydrotalcite decreased the gastric injury in the mucosa of stomach significantly (7±4.5 vs. 16±11.25, 1.5±2 vs. 2.5±6; P<0.01, P<0.05). The levels of EGF and PGE2 in blood serum were markedly higher in hydrotalcite group than that in model group and ranitidine group in preventive experiment (574.39±34.28 vs. 486.22±41.73, 488.07±24.44; P<0.01, P<0.01). The expression levels of COX-2 in gastric mucosa were also higher in hydrotalcite group than that in model group in both preventive and therapeutic experiments (12±4 vs. 9±6, 14±7 vs. 9±4; P<0.01, P<0.05). Conclusions. Hydrotalcite promotes gastric protection and healing via several mechanisms, including increased levels of PGE2 in blood serum, activation of EGF, and antagonising the inhibition of cyclooxygenase (COX) caused by NSAIDs.
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Ren, Shou-zhong, Jian-sheng Guo, Lin Sheng, Chen Jun, Shui-ping Dai, and Zhi-jian Ma. "PROTECTIVE EFFECT OF FENGLIAO-CHANGWEIKANG EXTRACTS, A TRADITIONAL CHINESE HERBAL MEDICINE FORMULA,ON MUCOSA IN RAT WITH CHRONIC GASTRITIS." African Journal of Traditional, Complementary and Alternative Medicines 13, no. 1 (December 3, 2015): 53–61. http://dx.doi.org/10.21010/ajtcam.v13i1.8.

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Background: Fengliao-Changwei-Kang(FCK), Chinese patent drug, is a famous traditional Chinese herbal medicine formula, which is effectively used to cure gastrointestinal disease including gastritis, enteritis and diarrhea in the clinic for many years. However, little research has been focused on the protective effects of FCK on the gastric mucosa of chronic gastritis (CG) model rat. Objective: The present study aimed to explore the effects of FCK extract on mucosa in rats with Chronic Gastritis. Materials and Methods: The CG rat model was induced by synthetic methods. The serum levels of EGF was measured by enzyme linked immunosorbent assay(ELISA) method, the expression of growth factor receptor (EGFR) in gastric mucosa was detected by immunohistochemical method, the mRNA expressions of NF-κB p65 was detected in-situ hybridization. Results: In the model group, the inflammation grades of gastric mucosa and the expressions of NF-κB p65 mRNA in gastric mucosa were markedly higher than those of the control group (P0.05). Conclusions: FCK extract could alleviate mucosal inflammation by down regulating the expressions of NF-κB p65 mRNA and promote tissue repair by up regulating EGFR expression in gastric mucosa cell.
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Villa, Afonso Luiz, Ceneviva Reginaldo, Fernanda Viaro, Fernando Ramalho, Antonio Dorival Campos, and Paulo Roberto B. Evora. "The cytoprotective effect of a nitric oxide donor drug on gastric mucous membrane of rats treated with ketoprofen, a non-steroidal anti-inflammatory drug." Arquivos de Gastroenterologia 43, no. 3 (September 2006): 233–37. http://dx.doi.org/10.1590/s0004-28032006000300015.

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BACKGROUND: Non-steroidal anti-inflammatory drugs are considered today a very important group of medication, with a wide variety of therapeutic use, in different areas of modern medicine. Despite their beneficial effects on the patient, these drugs show a high incidence of side effects, mainly in the gastrointestinal tract. The physiopathological mechanisms of non-steroidal anti-inflammatory drugs induced lesions and the gastric mucosa defense mechanism became an important source for medical research, especially those which try to evaluate the role of nitric oxide as a cytoprotective agent. AIM: To define a possible cytoprotective effect of a nitric oxide donor, isosorbide dinitrate, on the gastric mucous of rats submitted to non-steroidal anti-inflammatory drugs ketoprofen treatment. METHODS: Adult male Wistar rats, previously submitted to starvation for 24 hours and divided in three groups: group I (standard): animals that received isotonic saline solution intragastric by gavage and intravenous. Group II (control-ketoprofen): animals that received isotonic saline solution intragastric by gavage and ketoprofen intravenous. Group III (nitrate/ketoprofen): animals that received 2mM solution of isosorbide dinitrate intragastric by gavage and ketoprofen intravenous. Later on, these animals were sacrificed and had their stomach removed and submitted to macroscopical, microscopical and biochemical studies. The evaluated parameters were: a) gastric lesion index; b) gastric mucous layer thickness; c) gastric tissue nitrate/nitrite (NOx) concentration and d) gastric tissue malondialdehyde concentration. RESULTS: a) Gastric lesion index evaluation showed a smaller statistically significant incidence on the animals of group III; b) group III showed a thicker mucous layer, which also was statistically significant, when compared to group II; c) the variation on tissue nitrate/nitrite concentration was similar in all three groups, without statistical significance when compared to each other. CONCLUSION: Isosorbide dinitrate has a cytoprotective activity on the gastric mucosa of rats submitted to ketoprofen action.
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Bakalarz, Dominik, Edyta Korbut, Zhengnan Yuan, Bingchen Yu, Dagmara Wójcik, Aleksandra Danielak, Katarzyna Magierowska, et al. "Novel Hydrogen Sulfide (H2S)-Releasing BW-HS-101 and Its Non-H2S Releasing Derivative in Modulation of Microscopic and Molecular Parameters of Gastric Mucosal Barrier." International Journal of Molecular Sciences 22, no. 10 (May 14, 2021): 5211. http://dx.doi.org/10.3390/ijms22105211.

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Hydrogen sulfide (H2S) is an endogenously produced molecule with anti-inflammatory and cytoprotective properties. We aimed to investigate for the first time if a novel, esterase-sensitive H2S-prodrug, BW-HS-101 with the ability to release H2S in a controllable manner, prevents gastric mucosa against acetylsalicylic acid-induced gastropathy on microscopic and molecular levels. Wistar rats were pretreated intragastrically with vehicle, BW-HS-101 (0.5–50 μmol/kg) or its analogue without the ability to release H2S, BW-iHS-101 prior to ASA administration (125 mg/kg, intragastrically). BW-HS-101 was administered alone or in combination with nitroarginine (L-NNA, 20 mg/kg, intraperitoneally) or zinc protoporphyrin IX (10 mg/kg, intraperitoneally). Gastroprotective effects of BW-HS-101 were additionally evaluated against necrotic damage induced by intragastrical administration of 75% ethanol. Gastric mucosal damage was assessed microscopically, and gastric blood flow was determined by laser flowmetry. Gastric mucosal DNA oxidation and PGE2 concentration were assessed by ELISA. Serum and/or gastric protein concentrations of IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-13, VEGF, GM-CSF, IFN-γ, TNF-α, and EGF were determined by a microbeads/fluorescent-based multiplex assay. Changes in gastric mucosal iNOS, HMOX-1, SOCS3, IL1-R1, IL1-R2, TNF-R2, COX-1, and COX-2 mRNA were assessed by real-time PCR. BW-HS-101 or BW-iHS-101 applied at a dose of 50 μmol/kg protected gastric mucosa against ASA-induced gastric damage and prevented a decrease in the gastric blood flow level. H2S prodrug decreased DNA oxidation, systemic and gastric mucosal inflammation with accompanied upregulation of SOCS3, and EGF and HMOX-1 expression. Pharmacological inhibition of nitric oxide (NO) synthase but not carbon monoxide (CO)/heme oxygenase (HMOX) activity by L-NNA or ZnPP, respectively, reversed the gastroprotective effect of BW-HS-101. BW-HS-101 also protected against ethanol-induced gastric injury formation. We conclude that BW-HS-101, due to its ability to release H2S in a controllable manner, prevents gastric mucosa against drugs-induced gastropathy, inflammation and DNA oxidation, and upregulate gastric microcirculation. Gastroprotective effects of this H2S prodrug involves endogenous NO but not CO activity and could be mediated by cytoprotective and anti-inflammatory SOCS3 and EGF pathways.
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Lyra, Anna, Markku Saarinen, Heli Putaala, Kaisa Olli, Sampo J. Lahtinen, Arthur C. Ouwehand, Mari Madetoja, and Kirsti Tiihonen. "Bifidobacterium animalisssp.lactis420 Protects against Indomethacin-Induced Gastric Permeability in Rats." Gastroenterology Research and Practice 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/615051.

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Gastrointestinal (GI) adverse effects such as erosion and increased permeability are common during the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Our objective was to assess whetherBifidobacterium animalisssp.lactis420 protects against NSAID-induced GI side effects in a rat model. A total of 120 male Wistar rats were allocated into groups designated as control, NSAID, and probiotic. The NSAID and probiotic groups were challenged with indomethacin (10 mg/kg−1; single dose). The probiotic group was also supplemented daily with 1010 CFU ofB. lactis420 for seven days prior to the indomethacin administration. The control group rats received no indomethacin or probiotic. The permeability of the rat intestine was analysed using carbohydrate probes and the visual damage of the rat stomach mucosa was graded according to severity.B. lactis420 significantly reduced the indomethacin-induced increase in stomach permeability. However, the protective effect on the visual mucosal damage was not significant. The incidence of severe NSAID-induced lesions was, nevertheless, reduced from 50% to 33% with the probiotic treatment. To conclude, theB. lactis420 supplementation protected the rats from an NSAID-induced increase in stomach permeability and may reduce the formation of more serious GI mucosal damage and/or enhance the recovery rate of the stomach mucosa.
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Bastaki, Salim MA, and John L. Wallace. "Pathogenesis of Nonsteroidal Anti-Inflammatory Drug Gastropathy: Clues to Preventative Therapy." Canadian Journal of Gastroenterology 13, no. 2 (1999): 123–27. http://dx.doi.org/10.1155/1999/738968.

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Gastric ulceration and bleeding are major impediments to the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs). The development of effective therapies for prevention of these adverse effects requires better understanding of their pathogenesis. Several features of NSAIDs contribute to the development of damage in the stomach, including the topical irritant effects of these drugs on the epithelium, impairment of the barrier properties of the mucosa, suppression of gastric prostaglandin synthesis, reduction of gastric mucosal blood flow and interference with the repair of superficial injury. The presence of acid in the lumen of the stomach also contributes to the pathogenesis of NSAID-induced ulcers and bleeding in a number of ways. Acid impairs the restitution process, interferes with hemostasis and can inactivate several growth factors that are important in mucosal integrity and repair. Profound suppression of gastric acid secretion has been shown to be effective in preventing NSAID-induced ulceration. There is a strong possibility that new NSAIDs entering the market will have greatly reduced toxicity in the gastrointestinal tract.
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Moghal, Naheed, and N. A. Jafarey. "Effects of Nonsteroidal Antiinflammatory Drugs on Gastric and Duodenal Mucosa." Gastroenterology 96, no. 2 (February 1989): 553–54. http://dx.doi.org/10.1016/0016-5085(89)91605-3.

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Dissertations / Theses on the topic "Gastric mucosa Effect of drugs on"

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黃尚行 and Sheung-hang Wong. "The gastric effects of ethanol and their modulation by drugs in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1989. http://hub.hku.hk/bib/B31232048.

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Wong, Sheung-hang. "The gastric effects of ethanol and their modulation by drugs in rats /." [Hong Kong] : University of Hong Kong, 1989. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12607757.

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Sennello, Kathleen Ann. "Comparison of the Effects of Deracoxib, Buffered Aspirin, and Placebo on the Gastric Mucosa of Healthy Dogs." Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/31788.

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This study tested the hypothesis that administration of deracoxib, a cyclooxygenase-2 specific (COX-2) inhibitor, would result in lower gastric lesion scores than administration of buffered aspirin and gastric lesion scores similar to placebo when administered to healthy dogs for 28 days. Twenty-four, healthy, random source dogs were divided into three groups. Group I received buffered aspirin, 23.6 mg/kg PO q 8h, group II received deracoxib, 1.6 mg/kg PO q 24h and placebo twice daily PO q 8h after deracoxib administration, and group III received placebo PO q 8h. Gastroscopy was performed on days -7, 6, 14, and 28 of treatment. Four regions of the stomach (pylorus, incisura, cardia, and body) were evaluated separately and lesions scored on a scale of 1 (mucosal hemorrhage) to 12 (perforating ulcer) by an observer unaware of which treatments the dogs received. Dogs were observed every 8 hours for vomiting, diarrhea and anorexia. Feces were scored from 1-5 (scores <4 were considered diarrhea).

Lesion scores for each group, at each location, and total scores, at each time period, were evaluated for the effects of time and treatment using a Kruskal-Wallis test. Total dog days of vomiting and dog days of diarrhea in each group were compared using a Wilcoxon rank sums test. Significance was determined at p<0.05.

Significantly higher median total gastric lesion scores were found in the aspirin group compared to the deracoxib or placebo groups on days 6, 14, and 28. There were no significant differences in median total gastric lesion scores between the deracoxib or placebo groups at any time during the study. There was no location effect on gastric lesion scores and there was no significant change in gastric lesion scores over time in any of the groups during treatment. Significantly more dog-days of vomiting occurred in the aspirin group as compared to the deracoxib group. No significant differences were found between groups for dog-days of diarrhea.

In this study, the administration of deracoxib to healthy dogs resulted in significantly lower gastric lesion scores compared to dogs receiving aspirin and lesion scores similar to those receiving placebo.
Master of Science

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Wong, Wing-hong. "The anti-ulcer mechanisms of Cortex moutan against stress-induced gastric mucosal damage in rats /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20265517.

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黃穎康 and Wing-hong Wong. "The anti-ulcer mechanisms of Cortex moutan against stress-induced gastric mucosal damage in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31221981.

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Stapleton, Graham Neil. "A study of the effects of sucralfate in the bile duct litigated pig peptic ulcer model with particular reference to the effects on the physico-chemical properties of gastric mucus and including comparisons with famotidine and misoprostol." Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/25727.

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Sucralfate is a drug that effectively heals duodenal, gastric and oesophageal ulcers. It is not absorbed systemically and it has been shown to act locally by coating the ulcer base. However when it was also shown to prevent stress ulcers and ethanolinduced gastric mucosa! lesions, it seemed likely that it acted in some way to improve the effectiveness of the gastric mucosa! barrier. Some investigators suggested that it did so by stimulating local prostaglandin release. The Slomiany group, on the basis of in vitro work on the effects of Sucralfate on pig gastric mucus, claimed that Sucralfate acted by altering the physico-chemical properties of mucus to increase the viscosity and retard the back diffusion of H+ ions. The work described in this dissertation set out to verify, in vivo, these claimed effects on mucus, using an experimental porcine model of peptic ulceration, the bile duct ligated pig. In addition, the effects of Sucralfate were compared with those of Famotidine and Misoprostol, and changes in mucous prostaglandins, gastric juice pepsin and gastric flora were sought. By way of introduction, the known and postulated actions of Sucralfate, current understanding of gastric mucus physiology and pathogenesis of peptic ulceration, have been reviewed, as have experimental animal models of peptic ulceration, in order to justify using the bile duct ligated pig model.
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Jeffrey, Stuart C. "Epidermal growth factor receptor in equine gastric stratified squamous mucosa : effect of progressive ulceration on receptor density /." Thesis, This resource online, 1996. http://scholar.lib.vt.edu/theses/available/etd-09182008-063547/.

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Lee, Adam Michael. "Impact of genetic and epigenetic variability in response to two test drugs 5-Flurouracil and Lansoprazole." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009p/lee.pdf.

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Dodridge, M. E. (Miles Edward). "The effects of variable dose methotrexate infusion in the laboratory rat." 1987. http://web4.library.adelaide.edu.au/theses/09DM/09dmd641.pdf.

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Hsin-min and 周欣敏. "The preventive effect of Mulberry anthocyanin extracts in diclofenac-induced rat gastric mucosa damage." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/76290790734319523055.

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碩士
中山醫學大學
生化暨生物科技研究所
97
Diclofenac is a NSAID drug which causes gastric mucosal lesion complication. Food bioactive compounds were reported could exert beneficial effects in the gastrointestinal tract. In this study, we evaluated whether Mulberry anthocyanin extracts (MAE) reduced Diclofenac-induced injury in the rat gastric mucosa. Rats were induced for gastric mucosal lesion with Diclofenac (DIC, 100 mg/kg, orally) after pretreated with MAE in various dosages (100mg/kg, 200mg/kg, 400mg/kg). A proton pump inhibitor, Esomeprazole, was used as a protection control. The gastroprotective effect of MAE was assessed by WBC count in whole blood and the activities of enzymatic antioxidants, such as glutathione-S- transferase (GST, GST α, GST π, GST μ isoforms ) in RBC .The levels of lipid peroxide, reduced glutathione (GSH), and protein expression of cyclooxygenase-2 (COX-2) in gastric mucosa were also evaluated. The stomach tissues were used for the histological examination. The results showed that pretreatment of MAE can significantly increase the activities of total GST, GST α, GST π, and GSH, and decrease the WBC number, lipid peroxidation, and protein expression of COX-2 as compared to DICtreated rats. Histological studies showed a consistent result as well as the antioxidative molecules described above. Taken together, MAE reduced Diclofenac-induced gastric mucosal lesion maybe due to its antioxidative characteristic and free radical scavenging activity, and it possesses a potential to act as gastroprotective agent.
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Books on the topic "Gastric mucosa Effect of drugs on"

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Rodolfo, Cheli, ed. Gastric protection. New York: Raven Press, 1988.

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Potent acid suppression-when is it appropriate? Royal Society of Medicine, 1990.

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Mozsik, Gyula, Andras Debreceni, and Kazuichi Okazaki. The Capsaicin- And Helicobacter Strains-Induced Cellular Mechanisms of the Gastric Mucosa in Animals and Humans. Akademiai Kiado, 2001.

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Daniel, Hollander, and Tytgat G. N. J, eds. Sucralfate: From basic science to the bedside. New York: Plenum Medical Book Co., 1995.

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(Editor), Daniel Hollander, and G. N. Tytgat (Editor), eds. Sucralfate: From Basic Science to Bedside. Springer, 1995.

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(Editor), C. H. Cho, and J. Y. Wang (Editor), eds. Gastrointestinal Mucosal Repair and Experimental Therapeutics (Frontiers of Gastrointestinal Research). S. Karger Publishers (USA), 2002.

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R, Cheli, ed. Gastric secretion: A physiological and pharmacological approach. Verona: Cortina International, 1986.

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Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that ghrelin is one of the crucial hormones deciphering the energy status required for the maintenance of organism homeostasis. Ghrelin acts as a signal of starvation or energy insufficiency and its level in plasma is reduced after the meal. Neuropeptide Y (NPY) and agouti-related peptide (AgRP; NPY/AgRP) neurons located in the arcuate nucleus (ARC) area are the main target of ghrelin in the hypothalamus. This subpopulation of neurons is indispensable for inducing orexigenic action of ghrelin. Moreover ghrelin acting as a neurohormone, mainly in the hypothalamus area, plays an important role in the regulation of growth and reproduction processes. Indeed, ghrelin action on reproductive processes has been observed in the systemic effects exerted at both hypothalamus-pituitary and gonadal levels. Similarly the GH-releasing ghrelin action was observed both on the hypothalamus level and directly on the somatotrophic cells in the pituitary and this dose-related GH releasing activity was found in in vitro as well as in in vivo experiments. In recent years, numerous studies revealed that ghrelin potentially takes part in the treatment of diseases associated with serious disturbances in the organism energy balance and/or functioning of the gastrointestinal tract. It was underlined that ghrelin may be a hormone with a broad spectrum of therapeutic effect on obesity and anorexia nervosa, as well as may also have protective effect on neurodegenerative diseases, inflammatory disorders or functional changes in the body caused by cancers. In overall, ghrelin treatment has been tested in over 100 preclinical studies with healthy volunteers as well as patients with various types of cancer, eating disorders such as anorexia nervosa and bulimia nervosa. It was observed that ghrelin has an excellent clinical safety profile and emerging side effects occurred only in 3–10% of patients and did not constitute a sufficient premise to discontinue the therapy. In general, it can be concluded that ghrelin may be sufficiently used as a prescription drug.
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Book chapters on the topic "Gastric mucosa Effect of drugs on"

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Collins, P. O., I. A. Tavares, and A. Bennett. "Inhibition of prostanoid synthesis by anti-inflammatory drugs in human gastric mucosa." In Side-Effects of Anti-Inflammatory Drugs, 97–100. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_8.

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Halter, F., A. Baumgartner, L. Varga, and H. R. Koelz. "Both E Prostaglandins and prolonged indomethacin treatment exert trophic effects on the gastric mucosa." In Side-Effects of Anti-Inflammatory Drugs, 133–42. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_12.

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Rowe, P. H. "Prostaglandins prevent red streaks in rat gastric mucosa caused by intravenous aspirin but not by salicylate." In Side-Effects of Anti-Inflammatory Drugs, 165–66. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_18.

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Leyck, S., A. M. Huther, and M. J. Parnham. "Polyene phosphatidylcholine: an inhibitor of NSAID gastric toxicity which increases impaired mucosal PGE2 synthesis." In Side-Effects of Anti-Inflammatory Drugs, 163–64. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_17.

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Ezer, E. "Evidence for sulphydryl-sensitive process in the mechanisms of acute gastric mucosal injury and defence." In Side-Effects of Anti-Inflammatory Drugs, 113–21. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_10.

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Konturek, S. J., J. Oleksy, and E. Zielonka. "Comparison of gastric mucosal damage and prostaglandin formation in arthritis patients treated with carprofen and ibuprofen." In Side-Effects of Anti-Inflammatory Drugs, 89–96. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_7.

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Warrington, S., N. Debbas, M. Farthing, M. Horton, A. Thillainayagam, and A. Umile. "Comparison of effects on gastrointestinal blood loss and gastric mucosal appearance of piroxicam-β-cyclodextrin, piroxicam and placebo." In Side-Effects of Anti-Inflammatory Drugs 3, 89–96. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2982-4_13.

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Gyires, K., C. Blandizzi, and M. Del Tacca. "Analysis of the Inhibiting Activity of Presynaptic α2-Adrenoceptors against NSAID-induced Gastric Mucosal Lesions in the Rat." In Side Effects of Anti-Inflammatory Drugs IV, 287–94. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5394-2_30.

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Szabo, S., E. Gyomber, R. E. Morales, L. Nagy, and P. Vattay. "Novel strategies of gastric and duodenal mucosal protection against NSAID injury: role of protease inhibitors, muscle relaxants and growth factors." In Side-Effects of Anti-Inflammatory Drugs 3, 115–25. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2982-4_15.

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Kromin, A. A. "Lesions of Gastric Mucosa under the Effect of Acute Emotional Stress." In Perspectives on Research in Emotional Stress, 191–204. London: Routledge, 2022. http://dx.doi.org/10.4324/9781315075488-15.

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Conference papers on the topic "Gastric mucosa Effect of drugs on"

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M.Hussein, Ali, Nadir Nanakali, and Mohammed M.Hussein. "EFFECT OF HYPERICUM PERFORATUM ON GASTRIC ULCER IN RAT." In 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.742.

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Gastric ulcer is a chronic condition that occurs when the mucosa of the stomach is broken. There is a physiological equilibrium between aggressive factors and mucosal defense. This study aimed to determine the prevention level and efficiency of herbal medicinal plants (Hypericum perforatum) and compared with the omeprazole drug.Many groups were prepared from Albino male rats, first control group (inoculate with H. pylori and fed with standard pellet), Second group, rats inoculated by H. pylori and prevented with aqueous extract H. perforatum in two dosages (250mg/kg, 500mg/kg), Third group inoculated by H. pylori and prevented with standard drug omeprazole at the dose (20mg/kg).The result showed that H. perforatum inhibits (50.65%) stomach ulcer formation with a high dose. Omeprazole's' group results showed (24.50%) stomachs ulcer formation. Although the result of the current study improves, a high dosage of aqueous extracts of plants has more effectiveness than the low dosage of aqueous extracts of plants.
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Zhang, Lian, Sungkyoung Kim, Wenping Ding, Leizhen Zheng, Li Zhang, Yingying Tong, and Siyu Chen. "Abstract 5525: Antitumor effect of Realgar in combination with chemotherapy drugs on human gastric cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5525.

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Muguruma, Kazuya, Masakazu Yashiro, Hiroaki Tanaka, Kenjirou Kimura, Hisashi Nagahara, Ryousuke Amano, Eiji Noda, et al. "Abstract 100: The effect of synergic anti-proliferation of DNA methyltransferase inhibitor binding to anti-cancer drugs in gastric cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-100.

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Reports on the topic "Gastric mucosa Effect of drugs on"

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Xie, Yunhui, and Peng Pang. A Systematic Review and Network Meta-Analysis: Effect of of GLP-1 drugs on weight loss in obese people. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0074.

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Review question / Objective: 1、Whether GLP-1 drugs have weight loss effect on obese people ? 2、Which GLP-1 drugs are most effective in weight loss among obese people ? Condition being studied: Obesity is an important public health issue that has been on the rise over the last decades. It calls for effective prevention and treatment. Bariatric surgery is the most effective medical therapy for weight loss in morbid obesity, but we are in need for less aggressive treatments. Glucagon-like-peptide-1 receptor agonists are a group of incretin-based drugs that have proven to be productive for obesity treatment. Through activation of the GLP-1 receptor they not only have an important role stimulating insulin secretion after meals, but with their extrapancreatic actions, both peripheral and central, they also help reduce body weight by promoting satiety and delaying gastric emptying.
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