Journal articles on the topic 'Gastric mucosa Effect of drugs on'
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1
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.
Abstract:
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.
2
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.
Abstract:
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.
3
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.
Abstract:
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.
4
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.
Abstract:
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.
5
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.
Abstract:
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.
6
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.
Abstract:
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.
7
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.
Abstract:
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.
8
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.
Abstract:
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.
9
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.
Abstract:
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.
10
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.
11
Kononenko, N. N., M. T. Mirzaliev, and V. V. Chikitkina. "The effect of dry extract of cabbage garden on the local non-specific proteinase-inhibitory potential of the mucous membrane of the stomach on the model of acute gastric ulcer." Farmatsevtychnyi zhurnal, no. 6 (December 21, 2019): 77–84. http://dx.doi.org/10.32352/10.32352/0367-3057.6.19.09.
Abstract:
Peptic ulcer of the stomach and duodenum is a complex gastroenterological disease multifactorial in pathogenesis. One of the key components of non-specific inflammation in peptic ulcer disease is the activation of proteinases in the gastric mucosa and their interaction with proteinase inhibitors, which determines the degree of proteolytic aggression in terms of the development of destructive changes in the tissues that they damage.
The aim of the work was to study the effect of dry extract of cabbage garden on the components of the proteinase-inhibitor system in experimental gastric ulcer.
The effect of dry extract of cabbage garden on the local non-specific proteinase-inhibitory potential of the gastric mucosa was studied on the model of acute alcohol-prednisolone ulcers. Dry extract of cabbage garden at a dose of 50 mg/kg and comparison drugs – omeprazole and altan were administered intragastrically once a day for 7 days from the second day of the experiment. On the 8th day, elastase-like, trypsin-like activity and acid-stable inhibitors in the swabs from the stomach and intestines, biopsy samples of the gastric mucosa from the esophagus and fundus, and small intestine were determined.
It has been established that with an experimental alcohol-prednisolone gastric ulcer, a local non-specific proteinase-inhibitory system is involved in the mechanism of mucosal damage. At the same time, the level of trypsin-like and elastase-like activity of gastric juice increases and the activity of acid-stable inhibitors decreases, which normally suppress the enzymatic activity of proteinases. According to the effect on the non-specific proteinase-inhibitor system, the dry cabbage extract was significantly superior to altan and not inferior to omeprazole. The most pronounced effect of normalizing the activity of nonspecific proteinases and their inhibitors was established using a combination of dry cabbage extract with omeprazole. One of the mechanisms of the antiulcer action of the dry cabbage extract is its effect on the local nonspecific proteinase-inhibitory potential of the gastric mucosa.
In the model of acute alcohol-prednisolone gastric ulcer, dry extract of cabbage garden caused a decrease in the activity of local non-specific proteolytic enzymes and activation of proteinase inhibitors of the gastric mucosa and duodenum, exceeding the activity of altan. Under the combined use of the dry extract of cabbage and omeprazole, a complete normalization of the state of the local non-specific proteinase-inhibitory potential of the gastroduodenal zone was observed.
12
Parkhomenko, V. V., І. М. Skrypnyk, І. І. Starchenko, and O. F. Gopko. "CHARACTERISTICS OF GASTRIC MUCOSA INJURY IN PATIENTS WITH NSAID-INDUCED GASTROPATHY AND CONCOMITANT ISCHEMIC HEART DISEASE, AND WAYS TO CORRECT THIS CONDITION." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 2 (July 6, 2020): 70–75. http://dx.doi.org/10.31718/2077-1096.20.2.70.
Abstract:
The non-steroidal anti-inflammatory drugs (NSAIDs) in general clinical practice can provoke the development of NSAID-induced gastropathy, which can be complicated by bleeding. The aim of this article was to evaluate the effect of eupatilin on histological changes of the gastric mucosa in patients with NSAID-induced gastropathy and concomitant ischemic heart disease depending on the association with Helicobacter pylori. The study included 125 patients with NSAID-gastropathy and concomitant stable ischemic heart disease I-II functional class. Patients were divided into two groups: I (n=82) included individuals with NSAID-gastropathy, which was not associated with H. pylori, while II (n=43) included individuals with H. pylori-induced gastropathy. Depending on the prescribed treatment complexes, patients were subdivided as follows: I-A (n=44) included patients, who took proton pump inhibitors in standard doses and II-A group (n=23) included patients, who received antihelicobacter therapy according to Maastricht V (2016) guidelines. Patients of groups I-B (n=38) and II-B (n=20) were additionally prescribed 60 mg of eupatilin (1 tablet) 3 times a day for 28 days. The upper endoscopy with the gastric mucosa biopsy, followed by histological examination was done at the beginning of treatment and in 45±2 days. The severity of gastric mucosa erosive and ulcerative injury was assessed endoscopically using a modified Lanzascore scale; morphological changes were evaluated by a semi-quantitative method on a visual-analogue scale. H. pylori is an independent and significant factor determining the severity of endoscopic and morphological changes in NSAID-gastropathy patients with concomitant ischemic heart disease. Acid-suppressive and antihelicobacter therapy can reduce the intensity of the structural injury of the gastric mucosa, but the identified changes substantiate the feasibility of long-term proton pump inhibitors prescribed to the patients with NSAID-gastropathy. Prescribing eupatilin against the background of basic therapy can significantly reduce the severity of erosive-ulcerative gastric mucosa injury assessed by Lanzascore scale while histomorphological parameters by reducing the activity of neutrophilic inflammation, protective effect on mucosal barrier resistance and microcirculatory condition.
13
Kim, Sun-Joong, Young Sam Park, Hyun-Dong Paik, and Hyo Ihl Chang. "Effect of anthocyanins on expression of matrix metalloproteinase-2 in naproxen-induced gastric ulcers." British Journal of Nutrition 106, no. 12 (June 23, 2011): 1792–801. http://dx.doi.org/10.1017/s000711451100242x.
Abstract:
Non-steroidal anti-inflammatory drugs cause gastric ulceration through a number of mechanisms including inhibition of PG synthesis, generation of reactive oxygen species (ROS) and induction of apoptosis. Recently, matrix metalloproteinases (MMP) have been suggested to play a crucial role in these mechanisms. The present study investigated the protective effect of anthocyanins isolated from black rice bran (Heugjinjubyeo) against naproxen-induced gastric mucosal injury in rats. The oral administration of anthocyanins (5, 25 or 50 mg/kg body weight) showed significant protection against naproxen (80 mg/kg body weight)-induced gastric ulcer and inhibited lipid peroxidation in the gastric mucosa. In addition, pretreatment with anthocyanins resulted in a significant increase in the activities of radical-scavenging enzymes such as superoxide dismutase, catalase and glutathione peroxidase. Also biochemical and zymographic analyses suggested that the administration of anthocyanins gives a significant protection against naproxen-induced gastric antral ulcer through scavenging ROS and regulation of matrix metalloproteinase-2 (MMP-2) activity. The results of intracellular radical activation show that anthocyanins suppress the generation of intracellular ROS and attenuate the suppression of MMP-2 activity by naproxen. These results suggest that anthocyanins extracted from black rice may offer potential remedy of gastric antral ulceration.
14
Tijani, Stephanie Abiola, Samuel B. Olaleye, and Ebenezer O. Farombi. "Anti-ulcerogenic effect of the methanol extract of Chasmanthera dependens (Hochst) stem on male Wistar rats." Journal of Basic and Clinical Physiology and Pharmacology 29, no. 4 (July 26, 2018): 377–83. http://dx.doi.org/10.1515/jbcpp-2017-0152.
Abstract:
AbstractBackgroundOxidative stress and free radical-mediated processes have been implicated in the pathogenesis of indomethacin-induced gastric ulcer. This study investigated the ability of the methanol extract ofChasmanthera dependensto protect the gastric mucosal from oxidative damage induced by oral administration of indomethacin in rats.MethodsTheC. dependensstems were chopped into pieces, air-dried, and pulverized into powder. One kilogram of the powder was macerated in 1 L of methanol for 72 h. The mixture was filtered and evaporated using rotatory evaporator to obtain the extract ofC. dependens. Adult male rats were divided into eight groups of six animals per group and were pretreated orally with the methanol extract ofC. dependens(200, 400, and 800 mg/kg) or cimetidine (CIM), a standard drug (50 mg/kg), for 7 days. Gastric ulcer was induced orally with indomethacin. Ulcerogenic parameters, oxidative stress indices, and histopathological examination of the stomach were assessed to monitor the gastroprotective potential ofC. dependensstem.ResultsIndomethacin caused severe gastric mucosa damage and significant reduction in the gastric mucosa antioxidant system with concomitant increase in the level of lipid peroxidation. Pretreatment with the methanol extract ofC. dependensor CIM significantly reduced the formation of ulcer at the different doses administered. Similarly, pretreatments with the extract or CIM improved the antioxidant system, decreased acid output, lipid peroxidation, and improved the architecture of the gastric mucosa in ulcerated rats.ConclusionsThe results show the gastroprotective effect of the methanolic extract ofC. dependens, which may be attributed to its antioxidant properties.
15
Wang, Caihui, Wen Su, Xingli Su, Guojun Ni, Tao Liu, and Yi Kong. "Synergy Effects of Three Plant Extracts on Protection of Gastric Mucosa." Natural Product Communications 10, no. 11 (November 2015): 1934578X1501001. http://dx.doi.org/10.1177/1934578x1501001146.
Abstract:
The gastric mucosa protection effect of three natural plant extracts, Hericium erinaceus (HE), Centella asiatica (CA) and Amomum villosum (AV), were evaluated using the indomethacin damage model. Compared with a single extract, a combination of HE/CA/AV, especially with the ratios of 80:10:10, 45:45:10 and 45:10:45, showed significant synergistic effects for protection of the gastric mucosa with gastric ulcer inhibition rates of 97.8 ± 0.7%, 86.5 ± 2.8% and 86.1 ± 3.6%, respectively. Microscopic appearances of the gastric mucosa were carried out to help confirm the results.
16
Liu, Xiao-Yu, Li-Fei Zheng, Yan-Yan Fan, Qian-Ying Shen, Yao Qi, Guang-Wen Li, Qi Sun, Yue Zhang, Xiao-Yan Feng, and Jin-Xia Zhu. "Activation of dopamine D2 receptor promotes pepsinogen secretion by suppressing somatostatin release from the mouse gastric mucosa." American Journal of Physiology-Cell Physiology 322, no. 3 (March 1, 2022): C327—C337. http://dx.doi.org/10.1152/ajpcell.00385.2021.
Abstract:
In vivo administration of dopamine (DA) receptor (DR)-related drugs modulate gastric pepsinogen secretion. However, DRs on gastric pepsinogen-secreting chief cells and DA D2 receptor (D2R) on somatostatin-secreting D cells were subsequently acquired. In this study, we aimed to further investigate the local effect of DA on gastric pepsinogen secretion through DRs expressed on chief cells or potential D2Rs expressed on D cells. To elucidate the modulation of DRs in gastric pepsinogen secretion, immunofluorescence staining, ex vivo incubation of gastric mucosa isolated from normal and D2R−/− mice were conducted, accompanied by measurements of pepsinogen or somatostatin levels using biochemical assays or enzyme-linked immunosorbent assays. D1R, D2R, and D5R-immunoreactivity (IR) were observed on chief cells in mouse gastric mucosa. D2R-IR was widely distributed on D cells from the corpus to the antrum. Ex vivo incubation results showed that DA and the D1-like receptor agonist SKF38393 increased pepsinogen secretion, which was blocked by the D1-like receptor antagonist SCH23390. However, D2-like receptor agonist quinpirole also significantly increased pepsinogen secretion, and D2-like receptor antagonist sulpiride blocked the promotion of DA. Besides, D2-like receptors exerted an inhibitory effect on somatostatin secretion, in contrast to their effect on pepsinogen secretion. Furthermore, D2R− /− mice showed much lower basal pepsinogen secretion but significantly increased somatostatin release and an increased number of D cells in gastric mucosa. Only SKF38393, not quinpirole, increased pepsinogen secretion in D2R− /− mice. DA promotes gastric pepsinogen secretion directly through D1-like receptors on chief cells and indirectly through D2R-mediated suppression of somatostatin release.
17
Antonenko, Antonina V., and Tetyana V. Beregova. "The improvement of treatment efficacy of gastropathy associated with the use of nonsteroidal anti-inflammatory drugs in Helicobacter pylori-negative patients with osteoarthritis." Current Issues in Pharmacy and Medical Sciences 27, no. 4 (December 1, 2014): 237–39. http://dx.doi.org/10.1515/cipms-2015-0023.
Abstract:
Abstract Among the more common side effects of osteoarthritis treatment are NSAID-gastropathy and NSAID-enteropathy. NSAIDs can cause direct injury to colon tissue and also impair synthesis of prostaglandins, reduce mucosal integrity, increase permeability and promote an influx of bacteria and toxins. Alterations in gastrointestinal permeability are considered as an initial step in the development of lesions of the gastric mucosa such as erosions and ulcers. The mechanisms underlying the ability of NSAIDs to cause ulceration in the stomach and proximal duodenum are well understood and this injury can be largely be prevented through suppression of gastric acid secretion. However, our work showed that 28-day administration of the anti-secretory preparation pantoprazole (20 mg 2 times per day) resulted in a statistically significant increase of dysbiosis. Monitoring of patients with osteoarthritis who used NSAIDs for more than three months showed that, in comparison to the situation before the beginning of treatment, changes in colonic microbiota were present. Multiprobiotic “Symbiter® acidophilic concentrated” introduced simultaneously with pantoprazole during 20 days prevented formation of dysbiotic changes and led to the quicker healing of gastric mucous healing, in comparison with patients who used only pantoprazole alone. Moreover, it brought about total healing of the gastric mucosa within 4 weeks from the beginning of treatment.
18
Fulga, Simona, Ana-Maria Pelin, Cristina Mihaela Ghiciuc, and Elena Cătălina Lupușoru. "Particularities of Experimental Models Used to Induce Gastric Ulcer." ARS Medica Tomitana 25, no. 4 (November 1, 2019): 179–84. http://dx.doi.org/10.2478/arsm-2019-0035.
Abstract:
Abstract Introduction: Gastric ulcer is one of the most common gastrointestinal diseases, therefore the constant interest for new treatments is due to adverse effects induced by current therapy. The restricted number of in vivo experimental models is a challenge for researchers. Objectives: Identifying the particularities of different types of experimentally induced gastric ulcer in laboratory animals to facilitate their choise for the study of new antiulcer drugs. Material and method: A search in PubMed and Scopus using keywords ( “experimentally” AND “gastric ulcer” AND “rats/mice”) to include experimental studies with the description of local-induced changes. Review articles and in vitro studies were excluded. Results and discussions: Experimental researches on new drugs for gastric ulcer use chemical or surgical methods to induce gastric lesions in rats. Non-steroidal anti-inflammatory drugs (NSAIDs) and acetic acid models to investigate antisecretory and cytoprotective effects; ethanol models evaluate cytoprotective and/or antioxidant effects; pylorus ligature models to evaluate the effects on the secretion of aggressive gastric factors (hydrochloric acid or pepsin). NSAIDs (indomethacin, acetylsalicylic acid or ibuprofen) inhibit cyclooxygenase activity, resulting from reduced mucus and bicarbonate secretion, decreased mucosal blood flow, alteration of microvascular structures, causing epithelial damage Ethanol enhances the proteolytic and hydrolytic action of hydrochloric acid and pepsin; in addition, stimulates the acid secretion and disruptes vascular endothelium. Pylorus ligature determines the accumulation of gastric acid resulting in gastric ulcers due to the autodigestion of the mucosa. Conclusion: The knowledge of the mechanisms to induce experimental gastric ulcers is essential for choosing the model to evaluate new antiulcer agents.
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Mazumder, Somnath, Rudranil De, Subhashis Debsharma, Samik Bindu, Pallab Maity, Souvik Sarkar, Shubhra Jyoti Saha, et al. "Indomethacin impairs mitochondrial dynamics by activating the PKCζ–p38–DRP1 pathway and inducing apoptosis in gastric cancer and normal mucosal cells." Journal of Biological Chemistry 294, no. 20 (April 2, 2019): 8238–58. http://dx.doi.org/10.1074/jbc.ra118.004415.
Abstract:
The subcellular mechanism by which nonsteroidal anti-inflammatory drugs (NSAIDs) induce apoptosis in gastric cancer and normal mucosal cells is elusive because of the diverse cyclooxygenase-independent effects of these drugs. Using human gastric carcinoma cells (AGSs) and a rat gastric injury model, here we report that the NSAID indomethacin activates the protein kinase Cζ (PKCζ)–p38 MAPK (p38)–dynamin-related protein 1 (DRP1) pathway and thereby disrupts the physiological balance of mitochondrial dynamics by promoting mitochondrial hyper-fission and dysfunction leading to apoptosis. Notably, DRP1 knockdown or SB203580-induced p38 inhibition reduced indomethacin-induced damage to AGSs. Indomethacin impaired mitochondrial dynamics by promoting fissogenic activation and mitochondrial recruitment of DRP1 and down-regulating fusogenic optic atrophy 1 (OPA1) and mitofusins in rat gastric mucosa. Consistent with OPA1 maintaining cristae architecture, its down-regulation resulted in EM-detectable cristae deformity. Deregulated mitochondrial dynamics resulting in defective mitochondria were evident from enhanced Parkin expression and mitochondrial proteome ubiquitination. Indomethacin ultimately induced mitochondrial metabolic and bioenergetic crises in the rat stomach, indicated by compromised fatty acid oxidation, reduced complex I– associated electron transport chain activity, and ATP depletion. Interestingly, Mdivi-1, a fission-preventing mito-protective drug, reversed indomethacin-induced DRP1 phosphorylation on Ser-616, mitochondrial proteome ubiquitination, and mitochondrial metabolic crisis. Mdivi-1 also prevented indomethacin-induced mitochondrial macromolecular damage, caspase activation, mucosal inflammation, and gastric mucosal injury. Our results identify mitochondrial hyper-fission as a critical and common subcellular event triggered by indomethacin that promotes apoptosis in both gastric cancer and normal mucosal cells, thereby contributing to mucosal injury.
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Myszor, M. F., and H. J. F. Hodgson. "The Effect of Nonsteroidal Anti-Inflammatory Drugs on Dna Synthesis in Human Gastric Mucosa." Clinical Science 70, s13 (January 1, 1986): 39P. http://dx.doi.org/10.1042/cs070039pa.
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Morozova, Olga Yu. "Non-steroidal anti-inflammatory drugs: Deleterious effect on the gastric mucosa and protection against ulcerogenic effects." Integrative Physiology 2, no. 4 (2022): 390–98. http://dx.doi.org/10.33910/2687-1270-2021-2-4-390-398.
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Yu, Lanlan, Ruijun Li, Wei Liu, Yalin Zhou, Yong Li, Yong Qin, Yuhan Chen, and Yajun Xu. "Protective Effects of Wheat Peptides against Ethanol-Induced Gastric Mucosal Lesions in Rats: Vasodilation and Anti-Inflammation." Nutrients 12, no. 8 (August 7, 2020): 2355. http://dx.doi.org/10.3390/nu12082355.
Abstract:
Alcohol consumption increases the risk of gastritis and gastric ulcer. Nutritional alternatives are considered for relieving the progression of gastric mucosal lesions instead of conventional drugs that produce side effects. This study was designed to evaluate the gastroprotective effects and investigate the defensive mechanisms of wheat peptides against ethanol-induced acute gastric mucosal injury in rats. Sixty male Sprague–Dawley rats were divided into six groups and orally treated with wheat peptides (0.1, 0.2, 0.4 g/kgbw) and omeprazole (20 mg/kgbw) for 4 weeks, following absolute ethanol administration for 1 h. Pretreatment with wheat peptides obviously enhanced the vasodilation of gastric mucosal blood vessels via improving the gastric mucosal blood flow and elevating the defensive factors nitric oxide (NO) and prostaglandin E2 (PGE2), and lowering the level of vasoconstrictor factor endothelin (ET)-1. Wheat peptides exhibited anti-inflammatory reaction through decreasing inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, and increasing trefoil factor 1 (TFF1) levels. Moreover, wheat peptides significantly down-regulated the expression of phosphorylated nuclear factor kappa-B (p-NF-κB) p65 proteins in the NF-κB signaling pathway. Altogether, wheat peptides protect gastric mucosa from ethanol-induced lesions in rats via improving the gastric microcirculation and inhibiting inflammation mediated by the NF-κB signaling transduction pathway.
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THONGSOM, Montakarn, Lanchakon CHANUDOM, and Jitbanjong TANGPONG. "Co-treatment Effect of Syzygium cumini (L.) Skeels on Indomethacin Induced Gastric Ulcer on Mice Model." Walailak Journal of Science and Technology (WJST) 16, no. 3 (December 1, 2019): 193–206. http://dx.doi.org/10.48048/wjst.2019.6224.
Abstract:
Syzygium cumini (L.) Skeels or SCC originally from India and Southeast Asia, commonly used as a medicinal and acted as antioxidant and anti-inflammatory plant. Indomethacin, which is a part of nonsteroidal anti-inflammatory drugs (NSAIDs) family, induced gastric damage and perforation through the excess generation of reactive oxygen species (ROS). This research focus on co-treatment administered between SCC and indomethacin in the subsequent 7 days and evaluated on oxidative damage, inflammatory parameter and epidermal growth factor (EGF) receptor. SCC showed a concentration and dose dependent reduction in ulcer index (UI) values leading to the increasing of inhibition percent when compared to indomethacin treated mice, confirmed by photographer which showed maximum efficacy on day 5 of treatment. On day 1 and day 3 of ulceration, malondialdehyde (MDA), oxidized glutathione (GSSG), nitrile contents and tumor necrosis factor-alpha (TNF-α) were increased. Gastric wall mucus and glutathione peroxidase (GPx) were down. After that gastric mucosa were recovered by healing processed and were regenerated the mucosal cap to promote EGF receptor. SCC was increased the up-regulation of COX-1 enzyme resulting in down-regulation to COX-2 expression at day 3 of ulceration. At day 5 and 7, the gastric ulceration were regenerated themselves. These all results indicated that SCC have a great protective effect against indomethacin induced gastric ulcer in in-vivo co-treatment model.
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Alhakamy, Nabil A., Shaimaa M. Badr-Eldin, Osama A. A. Ahmed, Abdulrahman A. Halwani, Hibah M. Aldawsari, Mohamed A. El-Moselhy, Aliaa Anter, et al. "Optimized Ellagic Acid–Ca Pectinate Floating Beads for Gastroprotection against Indomethacin-Induced Gastric Injury in Rats." Biomolecules 10, no. 7 (July 6, 2020): 1006. http://dx.doi.org/10.3390/biom10071006.
Abstract:
A peptic ulcer is an alimentary tract injury that leads to a mucosal defect reaching the submucosa. This work aimed to optimize and maximize ellagic acid (EA) loading in Ca pectinate floating beads to maximize the release for 24 h. Three factors were selected: Ca pectinate concentration (X1, 1–3 w/v %), EA concentration (X2, 1–3 w/v %) and the dropping time (X3, 10–30 min). The factorial design proposed eight formulations. The optimized EA–Ca pectinate formulation was evaluated for the gastric ulcer index and the oxidative stress parameter determination of gastric mucosa. The results indicated that the optimum EA–Ca pectinate formula significantly improved the gastric ulcer index in comparison with raw EA. The protective effect of the optimized EA–Ca pectinate formula was further indicated by the histopathological features of the stomach. The results of the study indicate that an EA formulation in the form of Ca pectinate beads would be effective for protection against gastric ulcers because of Nonsteroidal anti-inflammatory drugs (NSAID) administration.
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Renga, M., G. Brandi, G. M. Paganelli, C. Calabrese, S. Papa, A. Tosti, P. Tomassetti, M. Miglioli, and G. Biasco. "Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia." Gut 41, no. 3 (September 1, 1997): 330–32. http://dx.doi.org/10.1136/gut.41.3.330.
Abstract:
Background—The influence of gastrin on the colonic mucosa is still uncertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development.Aims—To evaluate the effect of gastrin on colorectal cell proliferation, patients with chronic endogenous hypergastrinaemia underwent proctoscopy. Biopsy specimens were taken in order to study rectal cell kinetics.Patients and controls—Ten patients with chronic autoimmune gastritis (CAG), six patients with Zollinger-Ellison syndrome (ZES), and 16 hospital controls took part in this study. Patients with CAG and ZES had basal serum gastrin concentrations significantly higher than controls (p<0.001).Methods—Immunohistochemistry was performed on 3 μm sections of rectal biopsy specimens incubated with 5′-bromodeoxyuridine.Results—The percentage of proliferating cells in the entire crypts (overall labelling index) was similar in all the groups. However, the labelling frequency in the upper two fifths of the glands (φh value) was significantly higher in patients with CAG or ZES compared with controls (p<0.01 in both patient groups versus controls).Conclusions—Endogenous hypergastrinaemia is associated with rectal cell proliferation defects, similar to those observed in conditions at high risk for colon cancer. The effect of the increased serum concentrations of gastrin on the colorectal mucosa after treatment with drugs inhibiting gastric acid secretion should be investigated.
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Lee, Ji Hwan, Hee Jae Kwak, Dongchul Shin, Hye Jin Seo, Shin Jung Park, Bo-Hee Hong, Myoung-Sook Shin, Seung Hyun Kim, and Ki Sung Kang. "Mitigation of Gastric Damage Using Cinnamomum cassia Extract: Network Pharmacological Analysis of Active Compounds and Protection Effects in Rats." Plants 11, no. 6 (March 8, 2022): 716. http://dx.doi.org/10.3390/plants11060716.
Abstract:
Gastritis is a common disease worldwide that is caused by various causes such as eating habits, smoking, severe stress, and heavy drinking, as well as Helicobacter pylori infections and non-steroidal anti-inflammatory drugs. Cinnamomum cassia is a tropical aromatic evergreen tree commonly used as a natural medicine in Asia and as a functional food ingredient. Studies have reported this species’ anti-obesity, anti-diabetic, and cardiovascular disease suppression effects. We evaluated the potential effects of C. cassia using non-steroidal anti-inflammatory drugs (NSAIDs), ethanol (EtOH), and ethanol/hydrochloric acid (HCl)-induced gastric mucosal injury models. C. cassia extracts reduced the area of gastric mucosa injury caused by indomethacin, NSAID, EtOH, and EtOH/HCl. We also applied a network pharmacology-based approach to identify the active compounds, potential targets, and pharmacological mechanisms of C. cassia against gastritis. Through a network pharmacology analysis, 10 key components were predicted as anti-gastritis effect-related compounds of C. cassia among 51 expected active compounds. The NF-κB signaling pathway, a widely known inflammatory response mechanism, comprised a major signaling pathway within the network pharmacology analysis. These results suggest that the anti-gastritis activities of C. cassia may be induced via the anti-inflammatory effects of key components, which suppress the inflammation-related genes and signaling pathways identified in this study.
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Paseban, Maryam, Saeed Niazmand, Mohammad Soukhtanloo, Naser T. Meibodi, Abbasali Abbasnezhad, Seyed M. Mousavi, and Mohammad J. Niazmand. "The Therapeutic Effect of Nigella sativa Seed on Indomethacin-induced Gastric Ulcer in Rats." Current Nutrition & Food Science 16, no. 3 (April 27, 2020): 276–83. http://dx.doi.org/10.2174/1573401315666190114152855.
Abstract:
Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used to relieve pain and reduce inflammation. However, gastric complications remain a major problem limiting their clinical usage. This study was carried out to evaluate the therapeutic effect of Nigella sativa seed (N. sativa seed) hydroalcoholic extract on indomethacin-induced gastric ulcer in rats and its possible mechanism. Methods: This study was carried out on forty-eight male Wistar rats. Gastric ulcer was induced by indomethacin (35 mg/kg). N. sativa seed extract (100, 200, and 400 mg/kg) and ranitidine (50 mg/kg) was administered orally for five days after ulcer induction. Ulcer index, gastric acid secretion, gastric mucus content, total thiol, malondialdehyde (MDA), and total hexose, and protein content in gastric juice were determined. Results: The ulcer index in groups of N. sativa seed was significantly lower as compared to indomethacin group. N. sativa seed significantly decreased MDA and protein content, but increased total thiol, total hexose, and mucus content as compared to indomethacin group. N. sativa seed did not affect gastric acid secretion. Conclusion: These findings showed that the gastroprotective effect of N. sativa seed against indomethacin- induced ulcer was mainly exerted by antioxidant activity, stimulation of gastric mucus secretion and also increased total hexose in the gastric mucosa.
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Chernikov, M. V., M. A. Oganova, A. S. Gerasimenko, and E. A. Artemyev. "ANTIULCER ACTIVITY OF DINITRATE 2-PHENYL-9DIETHYLAMINOETHYLAMINE[1,2-A]BENZIMIDAZOLE WITH HELICOBACTER PYLORI-LIKE DAMAGE OF GASTRIC MUCOSA." Pharmacy & Pharmacology 6, no. 4 (September 12, 2018): 367–79. http://dx.doi.org/10.19163/2307-9266-2018-6-4-367-379.
Abstract:
The search for new drugs providing effective and safe therapy of acid-dependent diseases of the gastrointestinal tract, continues to be an actual problem of modern pharmacotherapy. One of the most significant pathogenetic mechanisms of these diseases is associated with Helicobacter pylori damage to the gastric mucosa.The aim of this study is the experimental investigation of the antiulcer effect of 2-phenyl-9-diethylaminoethylamine [1,2-a] benzimidazole substance (hereinafter a Benzimidazole derivative substance) on the model of Helicobacter pylori-like gastric mucosal injury in combination with immobilization stress (a restraint).Materials and methods. For modeling a mucous membrane damage to experimental animals (white Wistar male rats), they were injected 120 mmol/l ammonia solution after a 24-hour immobilization stress (restraint). As reference drugs, the following officinal anti-ulcer drugs widely used in clinical practice, had been chosen: Rranitidine (30 mg/kg, 10 mg/kg and 3 mg/kg) and Omeprazole (3 mg/kg, 1 mg/kg and 0.3 mg/kg). The study substance was used in the doses of 30 mg/kg, 10 mg/kg and 3 mg/kg. The maximum doses of the reference drugs were calculated on the basis of maximum daily doses for humans, taking into consideration the interspecies conversion factor. The maximum dose of the substance under study was selected experimentally. The logarithmic dose range was used for the convenience of further calculations of the ED50 value. All the studied objects were introduced intragastrically through a non-traumatic tube.Results and discussion. It has been established that the studied substance significantly reduced the area of mucosal damage relative to the control values in modeling Helicobacter pylori-like gastric mucosal injury provoked by the administration of ammonia solution against the background of gastric mucosal ischemia after a 24-hour restraint. At the same time, the inhibition of ulceration reached 78%, while in the groups receiving Ranitidine and Omeprazole, it reached 66% and 50%, respectively. The calculated ED50 values were the following: for the substance under study – 16.03 mg/kg, and for Ranitidine – 15.99 mg/kg.Conclusion. The gained results indicate that the studied Benzimidazole derivative is superior to analogs in its ability to suppress gastric mucosal ulceration provoked by Helicobacter pylori-like gastric mucosal injury, which confirms the relevance of further study of anti-ulcer activity and the development of the pharmaceutical dosage form based on it.
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Wróblewski, Hubert, and Aleksandra Zimna. "Proton pump inhibitors usage and the risk of cancer." Journal of Education, Health and Sport 11, no. 8 (August 28, 2021): 342–48. http://dx.doi.org/10.12775/jehs.2021.11.08.038.
Abstract:
Introduction and purpose of the work:Proton pump inhibitors are used to reduce gastric acidity by irreversibly inhibiting the hydrogen-potassium ATPase present in the parietal cells of the stomach. These drugs are used more and more often, often not in accordance with the recommendations. There are reports suggesting a relationship between chronic PPI use and the occurrence of cancer. The aim of the study is to present information on the relationship between the use of proton pump inhibitors and the risk of developing cancer.State of knowledge:Recent field studies have shown that there is a significant relationship between PPI use and carcinogenesis. One possible mechanism is related to the sustained release of gastrin in large amounts, which in turn stimulates the production of substances with trophic effects on the gastrointestinal mucosa, and cell proliferation over time may lead to cancer formation. The relationship between high gastrin concentration and the formation of gastric neuroendocrine neoplasms, tumors of the liver, pancreas and esophagus has been proven.Summary:Proton pump inhibitors are considered safe drugs. Taking into account the described reports on the increased risk of developing certain cancers, when prescribing PPIs, the risk associated with their use should also be taken into account. However, it seems that the benefits of using these drugs outweigh the risks in most cases.
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Balasubramanian, T., M. Somasundaram, and A. John William Felix. "Taurine Prevents Ibuprofen-Induced Gastric Mucosal Lesions and Influences Endogenous Antioxidant Status of Stomach in Rats." Scientific World JOURNAL 4 (2004): 1046–54. http://dx.doi.org/10.1100/tsw.2004.207.
Abstract:
Recently, free radicalinduced tissue damage is implicated in the nonsteroidal anti-inflammatory drugs (NSAIDs)involved gastric mucosal lesion. Administration of taurine, an endogenous antioxidant, is reported to be beneficial in various clinical conditions. Therefore, we decided to study the protective effect of taurine in ibuprofen-induced gastropathy and the effects of administration of taurine on the endogenous antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX), and reduced glutathione (GSH) of stomach. In rats, administration of taurine orally for three consecutive days (250 mg/kg body weight) protected the gastric mucosa from ibuprofen-induced, acute gastric mucosal lesion. In ibuprofen-treated rats, the lipid peroxidation measured as thiobarbituric acid reactive substances (TBARS), a marker for free radicalinduced tissue damage, is also significantly decreased by taurine. Ibuprofen treatment resulted in a significant increase in the activities of total SOD, manganese SOD (Mn-SOD), and GPX and reduced GSH. Taurine administration in ibuprofen-treated rats also showed a significant increase in the activities of the antioxidant enzymes namely total SOD, Mn-SOD, GPX, CAT, and the level of reduced GSH. The activity of copper-zinc SOD enzyme (Cu-Zn SOD) is not affected by ibuprofen or taurine. There is no temporal relation between the antioxidant status of the stomach and the tissue damage following oral administration of ibuprofen or taurine.
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Danielewski, Maciej, Sylwia Zielińska, Agnieszka Matuszewska, Wojciech Słupski, Maciej Włodarczyk, Izabela Jęśkowiak, Benita Wiatrak, et al. "Sanguinarine-Chelerythrine Fraction of Coptis chinensis Exerts Anti-inflammatory Activity in Carrageenan Paw Oedema Test in Rats and Reveals Reduced Gastrotoxicity." Oxidative Medicine and Cellular Longevity 2022 (March 16, 2022): 1–12. http://dx.doi.org/10.1155/2022/1504929.
Abstract:
Inflammatory diseases are a common therapeutic problem and nonsteroidal anti-inflammatory drugs are not deprived of side effects, of which ulcerogenic activity is one of the most frequent. The aim of the study was to evaluate the anti-inflammatory activity of the sanguinarine-chelerythrine (SC) fraction of Coptis chinensis and its influence on the integrity of gastric mucosa. The study was conducted on sixty male rats randomly divided into six experimental groups: two control groups (a negative control group CON and a positive control group CAR); three groups receiving an investigational fraction of C. chinensis (1, 5, 10 mg/kg i.g.) named SC1, SC5, and SC10, respectively; and a group receiving indomethacin (IND) (10 mg/kg i.g.) as a reference drug. In all animals, the carrageenan-induced paw oedema was measured; PGE2 release, TNFα production, and MMP-9 concentration in inflamed tissue were determined. Additionally, the macroscopic and microscopic damage of gastric mucosa was evaluated. Administration of SC dose-dependently inhibited the second phase of carrageenan rat paw oedema and PGE2 release, decreased the production of TNFα, and reduced the concentration of MMP-9, and the efficacy of the highest dose was comparable to the effect of IND. Contrary to IND, no gastrotoxic activity of SC was detected. The investigated sanguinarine-chelerythrine fraction of C. chinensis seems to be a promising candidate for further research on new anti-inflammatory and analgesic drugs characterized with a safer gastric profile compared to existing NSAIDs.
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Koshurba, I. V., F. V. Hladkykh, and M. O. Chyzh. "EVALUATION OF ANTIULCEROGENIC EFFECT OF CRYOCONSERVATED PLACENTA EXTRACT ON THE MODEL OF ETHANOL-PREDISONOLIC LESIONS OF THE GASTRIC MUCOSA." Medical Science of Ukraine (MSU) 18, no. 2 (June 30, 2022): 3–9. http://dx.doi.org/10.32345/2664-4738.2.2022.01.
Abstract:
Relevance. Gastric and duodenal ulcers occur in 6-10% of the adult population, and mortality from peptic ulcers ranges from 5 to 15%. Conservative treatment of this disease almost always involves the use of antisecretory and antibacterial drugs. Existing treatment regimens for peptic ulcer disease, focused on key pathogenetic mechanisms, do not take into account the individual adaptive and trophological characteristics of patients. As a potential antiulcer agent, our attention was drawn to the cryopreserved placenta extract ("Cryocell-cryoextract placenta"). It eliminates the ulcerogenic effect of anti-inflammatory drugs of non-steroidal nature, without affecting their therapeutic efficacy.
Objective: to characterize the anti-ulcerogenic effect of therapeutic and prophylactic use of cryopreserved placenta extract in the model of alcohol-prednisolone gastric lesions in rats.
Methods. The study was performed on 28 male rats weighing 200-220 g. they were randomized into four groups: I (n = 7) – intact rats, II (n = 7) – control – rats with model pathology (alcohol-prednisolone gastric lesion) without treatment, III (n = 7) – rats with alcohol-prednisolone gastric lesions, which were injected with cryoextract placenta (0.16 ml / kg body weight, intramuscularly), IV (n = 7) – rats with alcohol-prednisolone gastric lesions, which were administered the reference drug esomeprazole, proton pump inhibitor (50 mg / kg , intragastric). Gastric lesions in rats were simulated by intragastric single administration of prednisolone (20 mg/kg) dissolved in 80.0% ethanol (0.6 ml/100 g body weight). Cryoextracts of the placenta were administered intravenously in a prophylactic mode – 1 time per day for 4 days before and 1 time 60 minutes after the introduction of ethanol-prednisolone mixture. In 24 h. after administration of the mixture, rats were removed from the experiment and the size of the stomach (bloating) and the presence of adhesions with adjacent organs were evaluated macroscopically by the following criteria: erosions and hemographies, hyperemia, edema and mucosal fold disorders. For each group, the percentage of experimental animals was calculated according to these characteristics and the average value of their severity. The values of the ulcer index were calculated for each group.
Results. The study showed that the introduction of placental cryoexact as well as the reference drug esomeprazole led to a statistically significant (p<0.05) reduction of three times the prevalence of gastric ulcers in rats after administration of alcohol-prednisolone mixture. The use of placental cryoextract in the treatment-and-prophylactic regimen led to a statistically significant (p<0.05) decrease in the value of the ulcer index in 13 times relative to the control rats, and the average score of macroscopic assessment of gastric mucosa was 3.5 times lower and was 1.1±0.24 and 3.9±0.26, respectively. In animals treated with esomeprazole 2 times more moderate (2 [0.5; 3] points) hyperemia of the central nervous system (57.1% and 28.6%, respectively) and several times more moderate (2 [0; 2]). points) edema of the secondary school. In addition, edema of the central nervous system in rats administered esomeprazole led to a clear (3 [2; 3] points) violation of the folding of the central nervous system in 71.4% of rats. In contrast to the use of esomeprazole, placental cryoextract more significantly leveled the hyperemia induced by the introduction of alcohol-prednisolone mixture and edema of the gastric mucosa, which were observed in only 28.6% and 14.3% of rats, respectively.
Conclusions. Therapeutic and prophylactic use of placental cryoextract was accompanied by statistically significant (p <0.05) comparable to esomeprazole antiulcer efficacy in the model of ethanol-prednisolone gastric lesion and amounted to 92.3%.
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MANOCHA, Sachin, Dushyant LAL, and Subramanian VENKATARAMAN. "ADMINISTRATION OF H2 BLOCKERS IN NSAID INDUCED GASTROPATHY IN RATS: effect on histopathological changes in gastric, hepatic and renal tissues." Arquivos de Gastroenterologia 53, no. 1 (March 2016): 36–43. http://dx.doi.org/10.1590/s0004-28032016000100008.
Abstract:
ABSTRACT Background Nonsteroidal anti-inflammatory drugs induces gastric mucosal lesions because of its acidic properties. Ranitidine, an H2 receptor antagonist, has proved beneficial in patients with gastric ulcers. Objective The present study was performed to assess the effect of administering ranitidine in Nonsteroidal anti-inflammatory drugs (diclofenac, nimesulide) induced gastropathy, and their effect on the histopathology of stomach, kidney and liver. Methods Diclofenac, nimesulide, and ranitidine were administered in doses of 2, 4, and 6 mg/kg, p.o. once daily for 14 days, and their effect on gastric volume, acidity, mean ulcer number, and gastric pH. In addition, histopathological examination was also performed on sections of stomach, kidney and liver. Results Following the administration of diclofenac or nimesulide, all the gastric parameters were significantly altered as well as the histopathology of stomach, liver and kidney. In the control group, the renal sections showed normal glomeruli with no thickening of glomerular basement membrane, while in diclofenac alone, nimesulide alone, and ranitidine with nimesulide groups, the thickening of glomerular basement membrane was observed. These alterations were observed to be reversed in the ranitidine with diclofenac group. In the sections from the liver, the control group showed anastomosing plates and cords of cuboidal hepatocytes with round well stained nuclei and abundant cytoplasm. In the ranitidine with diclofenac, and ranitidine with nimesulide groups, mild dilatation of sinusoids is seen coupled with prominence of central vein. In the diclofenac alone and nimesulide alone groups, the proximal and distal convoluted tubules show mild focal tubular necrosis. In the gastric sections, the control group showed several folds forming villi, and the epithelial lining surface of the mucosa. In the ranitidine with diclofenac, and ranitidine with nimesulide groups, the duodenum showed scattered inflammatory cells composed predominantly of lymphocytes. In diclofenac alone and nimesulide alone group, the sections from the gastric areas showed partial necrosis and mild chronic inflammation respectively. Conclusion The study, therefore, has provided therapeutic rationale towards simultaneous administration of H2 receptor blocker ranitidine with diclofenac to be more beneficial as compared to ranitidine with nimesulide, to minimise the gastric intolerance of diclofenac in long term treatment of inflammatory conditions.
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Husori, Dadang Irfan, Marianne Marianne, Nabila Deli Syafarina Lubis, Kurnia Lavinda Yusfa, and Intan Farah Diba Angela. "Evaluation of Gastroprotective Effect from Phaleria macrocarpa Fruits Extract on Gastric Ulcer in Male Wistar Rats." Open Access Macedonian Journal of Medical Sciences 10, A (March 15, 2022): 462–69. http://dx.doi.org/10.3889/oamjms.2022.8242.
Abstract:
Abstract
BACKGROUND: The long-term use of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) triggers gastric mucosal damage and causes ulcers. Meanwhile, studies showed that God's crown fruit (Phaleria macrocarpa) contains secondary metabolites of flavonoids and tannins that can protect the gastric mucosa.
AIM: This study aims to determine the gastroprotective effect of P. macrocarpa ethanolic extracts against gastric ulcers in rats induced with acetosal and ethanol. The extracts were obtained by maceration method using 96% ethanol as solvent.
METHODS: The male rats used were divided into 7 groups for each test with ethanol and acetosal induction. Each group consisted of 5 rats, namely normal control, induction, carrier, positive control (sucralfate 360 mg/kg BW and omeprazole 3.6 mg/kg BW), and extract doses 100, 200, and 400 mg/kg body weight. All groups were given treatment for 7 days except normal and induction controls. On day 6, rats were fasted for 36 hours and induced with acetosal/ethanol. In ethanol induction, the animal was sacrificed after 10 hours of immersion while in acetosal, the animal was sacrificed 6 hours later. The stomach section was taken for macroscopic, microscopic parameters and gastric acid secretion examination.
RESULTS: The results of phytochemical screening showed that the extract contained flavonoids, tannins, saponins, alkaloids, and glycosides. In acetosal-induced ulcers, the administration of one dose of the extract reduced the number and score of ulcers, repair epithelial cells, increase pH, and total gastric acidity. Furthermore, the percentage of ulcer inhibition at the extract dose of 400 mg/kg BW was 91.91±3.74% in ethanol induction, and 59±13.08% in acetosal.
CONCLUSION: The ethanolic extract of P. macrocarpa has a gastroprotective effect on acetosal-induced gastric ulcer rats.
Keywords: Phaleria macrocarpa, Mahkota Dewa fruit, gastroprotective, gastric ulcers, extract
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Rahmadi, Mahardian, Nily Su’aida, Pratiwi Yustisari, Wahyu Agung Dewaandika, Elma Oktavia Hanaratri, Mareta Rindang Andarsari, Sumarno, and Toetik Aryani. "Gastroprotective effect of fluvoxamine and ondansetron on stress-induced gastric ulcers in mice." Journal of Basic and Clinical Physiology and Pharmacology 32, no. 4 (June 25, 2021): 485–90. http://dx.doi.org/10.1515/jbcpp-2020-0424.
Abstract:
Abstract Objectives The association between stress and gastric ulcers has been well reported. This study is divided into two parts: the first part of this study is consisted of analyzing the effect of fluvoxamine administration by intracerebroventricular (ICV) and intraperitoneal (IP) injections on stress-induced gastric ulcers. The second part investigates the effect of ondansetron in influencing the protection of the gastric mucous by giving fluvoxamine to the mice before being induced with stress. Methods Water immersion restraint stress (WIRS) was used to induce stress. Fluvoxamine 50 and 100 mg/kg by IP injection, fluvoxamine 9.3 µg, and 18.6 µg by ICV injection 30 min before the induction of stress. Meanwhile, single drug and in combination administered to the mice, ondansetron 3 mg/kg was given by IP at 60 min, and fluvoxamine 50, 100 mg/kg orally at 30 min before stress induction. Results The obtained results show fluvoxamine 50 and 100 mg/kg by IP, and fluvoxamine 18.6 µg by ICV had significantly reduced ulcer index with p<0.005, p<0.001, and p<0.005 while fluvoxamine 9.3 µg showed the insignificant result. Fluvoxamine 50 mg/kg, fluvoxamine 100 mg/kg, and ondansetron 3 mg/kg monotherapy have a significant reduction in ulcers with p<0.005, p<0.001, and p<0.05, while the combination drugs showed an insignificant reduction in ulcers. Conclusions Fluvoxamine with different administration routes and ondansetron monotherapy before stress reduce the occurrence of gastric ulcers, while the combination drugs did not increase the protective effect of the gastric mucosa.
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Ige, Serah Funke, Bolade S. Olateju, Victor A. Oladipupo, Adedayo T. Adekola, and Oluwaseun B. Ademilua. "Role of Low Environmental Temperature in Peptic Ulcer Development." International Journal of Medical Research & Review 9, no. 3 (May 31, 2021): 193–204. http://dx.doi.org/10.17511/ijmrr.2021.i03.10.
Abstract:
Peptic ulcers are described as acid-induced lesions found in the stomach and duodenum caused bythe imbalance between the defending factors of the mucosa and the attacking factors such ashydrochloric acid in gastric juice, with Helicobacter Pylori (H. Pylori) and Non-Steroidal Anti-Inflammatory Drugs NSAIDs. They exhibit seasonal patterns in their occurrence, with higheroccurrence in winter and spring and a low occurrence in summer. Temperature plays a major role intheir occurrence, some of which have resulted in increased morbidity in some number of diseases,such as gastrointestinal bleeding, caused by an increase in air pressure, dry air (relative humidity)occurring from cold air, and also its actions on the protective effect helicobacter pylori in the humanbody. Their actions excite the adrenal gland marrow and the sympathetic nerve, causing rapidsecretion of adrenaline and non-adrenaline, angiotensin II and endothelin, resulting in damage tothe mucosa epithelial, caused by the contraction effect of the adrenal agents on the duodenalmucosa and blood vessel. It causes low expression of Epidermal Growth Factor Receptor (EGFR),Epidermal Growth Factor (EGF), Heat Shock Protein (HSP) 70, Occludin, Nitric Oxide Synthase(NOS), in the gastric mucosa, in extremely cold temperature than those in extremely hottemperature, increasing the gastric acid secretion in extremely cold temperature than in extremelyhot temperature. Therefore, this review aims to give general insight into the role of low temperaturein peptic ulcer development and further consideration in the treatment of peptic ulcer diseases.
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Afroz, Rumana, Md Ismail Khan, Kazi Afzalur Rahman, Mahbuba Jahan Lotus, Mir muhammad Shoyeb Shahabuddin, Tasnin Afrin, Nahid Yeasmin, and Kawsar Jahan Moon. "Histopathological Evaluation of Gastro Protective Effect of Trigonella Foenum Graecum Seed (Methi) and omeprazole in Experimentally Induced Gastric Ulcer in Rats." Journal of Dhaka Medical College 28, no. 1 (March 3, 2020): 67–75. http://dx.doi.org/10.3329/jdmc.v28i1.45759.
Abstract:
Context: Peptic ulcer is a common disorder of the stomach and duodenum. Bangladesh is a developing country with a very high point prevalence of duodenal ulcer disease (11.9%) and a H. pylori prevalence of more than 90% in asymptomatic adults and 80% in children at the age of 5 years. The multifactorial pathogenesis of peptic ulcers is secretion of gastric acid. The main therapeutic target is the control of this secretion using antacids, H2 receptor blockers (ranitidine, famotidine) or proton pump blockers (omeprazole and lansoprazole). However, nowadays, gastric ulcer therapy faces a major drawback because most of the drugs currently available in the market show limited efficacy against gastric diseases and are often associated with severe side effects. Thus, there is an urgent need to identify more effective and safe antiulcer agents. In this context, the use of medicinal plants for the prevention and treatment of different pathologies is in continuous expansion worldwide. From the ancient time, various plants were used in traditional medicine with reputation as efficacious remedies. The list of plant derived modern medicine is very long now. About 33% of the drugs produced in the developed countries are derived from plants. Trigonella foenum-graecum (Fenugreek, Methi) is one of them used in many parts of world. Preliminary study on animal showed that Trigonella foenum-graecum seed has significant gastro-protective effect. A study was carried out to demonstrate the gastro-protective effect of aqueous extract and ethanolic extract of Trigonella foenum-graecum seed (Fenugreek, Methi) and omeprazole on ethanol induced gastric ulcer in experimental rats.
Material and Methods: The present study was performed on 24 (twenty four) rats which were divided randomly into 4 groups each having 6 rats in the Pharmacology Department of Dhaka Medical college, Dhaka. 1 ml of absolute ethanol (5ml/kg body wt.) was orally administered to all groups by gastric intubations to induce gastric ulcer in all groups except normal control. Omeprazole suspension (20mg/kg body wt) was used as synthetic anti ulcer drug in study. Aqueous and ethanolic extract of Trigonella foenum-graecum seed(500mg/kg body wt) were used respectively orally. Histopathological analysis was carried out to evaluate the gastroprotective activity of aqueous and ethanolic extract of Trigonella foenum-graecum seed and omeprazole on ethanol induced gastric ulcer in experimental rats.
Result: Pretreatment with aqueous and ethanolic extract of Trigonella foenum-graecum seed (500mg/kg/body wt) showed very significant prevention in ethanol induced gastric ulcer. Results of the study showed that in case of ethanol treated rats gross examination showed a large amount of haemorrhagic lesions confined mostly in the gastric corpus. Histologically lesion involved about two-third of the mucosa layer and exfoliation of the mucosal cells was detected. Meanwhile, red blood cells were present in the gastric mucosa and edematous submucosa was discovered. However aqueous and ethanolic extract of Trigonella foenum-graecum seed significantly reduced the haemorrhagic lesions, tissue proliferation, infiltration of cells and sloughing induced by ethanol. This prevention was statistically very significant (P<0.001).
Conclusion: The aqueous and ethanol extracts of Trigonella foenum-graecum seed and omeprazole possess gastro protective properties.
J Dhaka Medical College, Vol. 28, No.1, April, 2019, Page 67-75
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Sugiharta, Amelia Dwi Nurulita, I. Gusti Ayu Trisna Windiani, I. Gusti Agung Ngurah Sugitha Adnyana, and I. Gusti Ayu Indah Ardani. "Erocive gastritis with bipolar affective disorder current episode severe depression with psychotic symptoms with history of sexual violence in adolescent." International journal of health & medical sciences 5, no. 4 (October 31, 2022): 313–16. http://dx.doi.org/10.21744/ijhms.v5n4.1995.
Abstract:
Depression is a mental health disorder characterized by feelings of sadness, unhappiness, hopelessness, and even guilt. Erosive gastritis is an erosion of the gastric mucosa caused by damage to the mucosal barrier that is superficial but does not penetrate the muscularis mucosal layer. The patient is a 17 year old girl. Experiencing sad behavior changes, lack of interest, loss of joy, and suicide attempts. In addition, the patient was vomiting blood, and was examined by a pediatric gastroenterohepatologist. The supporting examination that was carried out, namely endoscopy, showed that the patient had erosive gastritis. The patient was consulted to the psychiatry department because there was a history of psychiatric treatment due to a history of depression. The treatment provided includes psychoeducation, administration of antipsychotic drugs quetiapine and valproic acid, as well as drugs for erosive gastritis including Sucralfate and Omeprazole. Episodes of major depression with psychotic symptoms can cause erosive gastritis in adolescents. Stress affects physiological effects, via the HPA-axis pathway.
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Suchitra M R, Danalakshmi G K, Sampathkumar P, Sumathi S, Poornima A, and Parthasarathy S. "A study of In vitro antioxidant and apoptotic effect of citrus medica Linn. leaves (Naarthai) against human gastric adenocarcinoma cell line (ags)." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (December 21, 2020): 1188–91. http://dx.doi.org/10.26452/ijrps.v11ispl4.4263.
Abstract:
Carcinoma or cancer of the stomach is one of the common malignancies of older men. Numerous methods of treatment options, including herbal and plant products, have been described for its management. The leaves of citrus medica or the naarthai leaves as it has been named traditionally do possess activities in the gastric mucosa. Hence, we decided to extract the phytochemicals from the leaves and find out the antioxidant, cytotoxic potential of the same. After confirmation of the leaves from appropriate authorities, petroleum ether, ethanolic and aqueous extracts of the leaves were made. The IC 50 was found to 200 micrograms and tested for cytotoxicity and apoptotic abilities in the AGS human gastric cell lines. The ethanolic extract showed maximal phytoconstituents. The aqueous extract showed 76.15% of scavenging effect, whereas the ethanolic extract showed 85.33% scavenging activity. Regarding the cytotoxicity effect of C. medica extract on the AGS cell line, it was observed that the percentage of cells was reduced to 50% in the treatment group when compared to the control group. The cells treated with ethanolic leaf extract of C. medica were arrested in G0-G1. Late apoptosis was significantly increased in the treated group when compared to the control group. The ethanolic leaf extracts of citrus medica possessed antioxidant and anti-cancer properties in gastric mucosal lines. This option can be considered for further production of drugs from such plants.
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Hawkey, C. J., A. B. Hawthorne, N. Hudson, A. T. Cole, Y. R. Mahida, and T. K. Daneshmend. "Separation of the impairment of haemostasis by aspirin from mucosal injury in the human stomach." Clinical Science 81, s25 (October 1, 1991): 565–73. http://dx.doi.org/10.1042/cs0810565.
Abstract:
1. An increasing body of data suggests that the anti-haemostatic as well as the ulcerogenic actions of aspirin and other non-steroidal anti-inflammatory drugs may be operative when patients present with haematemesis and melaena. 2. We therefore developed methods to allow separate evaluation of the erosive and anti-haemostatic actions of aspirin in the human gastric mucosa. Volunteer subjects took 300 mg of aspirin daily in the morning or 600 mg of aspirin four times a day for 5 days under blinded randomized conditions. Changes in spontaneous gastric microbleeding, endoscopic signs of injury, spontaneous bleeding per gastric erosion, biopsy-induced bleeding and eicosanoids were studied. 3. Both doses of aspirin significantly inhibited gastric mucosal synthesis of prostaglandin E2 and reduced the serum thromboxane concentration. Erosions developed and regressed rapidly; compared with baseline 300 mg of aspirin daily in the morning caused substantial numbers of gastric erosions to develop (mean 5.3, 95% confidence limits 2.7–10.2) but this was significantly less than that caused by 600 mg of aspirin four times a day (10.9, 7.2–16.5, P < 0.05). The presence of erosions was associated with enhanced spontaneous bleeding, but only during aspirin administration. 4. Aspirin significantly increased bleeding induced by mucosal biopsy and was associated with significant enhancements in the rate of bleeding per gastric erosion. Bleeding rate per erosion but not biopsy-induced bleeding showed a significant dose-related increase with 600 mg of aspirin four times a day. Enteric coating reduced endoscopic signs of injury, but did not affect the impaired haemostasis caused by aspirin. 5. We conclude that aspirin can be shown to have both erosive and anti-haemostatic effects in the human stomach. Each can be evaluated separately in our model system. Both are potential therapeutic targets for the prevention of major upper-gastrointestinal bleeding caused by aspirin and probably other non-steroidal antiinflammatory drugs.
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Bibik, E. Yu, A. V. Myazina, K. A. Frolov, V. V. Dotsenko, and S. G. Krivokolysko. "Impact of new 1,4‑dihydrothiopyridine derivatives with analgesic activity on gastric mucosa." Glavvrač (Chief Medical Officer), no. 9 (August 31, 2022): 16–18. http://dx.doi.org/10.33920/med-03-2209-04.
Abstract:
In clinical practice, the occurrence of such a side effect as gastrotoxicity can occur in patients taking NSAIDs with any route of administration. In this case, damage not only to the upper parts of the digestive tract is noted, but also to the intestine as a whole, since NSAID-induced enteropathy is manifested by the intestinal permeability disorder with protein exudation and diapedesis of erythrocytes, as well as by the development of erosions, ulcers, and life-threatening complications: bleeding, perforation, intestinal obstruction, and the appearance of circular folds [1]. The purpose of the study: to investigate the morphofunctional state of the stomach after exposure to non-steroidal anti-inflammatory drugs and novel heterocyclic compounds synthesized by us which have been proven to have high analgesic activity in white rats.
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Khémiri, Ikram, and Lotfi Bitri. "Effectiveness of Opuntia ficus indica L. inermis Seed Oil in the Protection and the Healing of Experimentally Induced Gastric Mucosa Ulcer." Oxidative Medicine and Cellular Longevity 2019 (November 15, 2019): 1–17. http://dx.doi.org/10.1155/2019/1568720.
Abstract:
Gastric ulcer is a painful lesion of the gastric mucosa which can be disabling, or even more very serious in the case of a perforation of the stomach and internal hemorrhage. Traditional pharmacopeias have shown the efficacy of various plant extracts in the treatment of this pathology. Some extracts from Opuntia ficus indica (OFI) have been proven to have medicinal therapeutic benefits. The aim of this study was to investigate the preventive and curative effects of OFI seed oil extracted by cold pressing on an ethanol-induced gastric ulcer model in rats. Gastroprotective activities of the oil were assessed as pretreatments prior to ethanol gavage of Wistar rats compared to reference drugs. Two oil dose effects were tested. Ulcer and gastric parameters were measured (ulcerated areas (mm2), % of ulcer inhibition, gastric juice volume and pH, and mucus weight). Macroscopical and microscopical assessments of the stomachs as well as gastric biopsy histological studies were carried out. OFI oil exhibited a high efficiency in the protection of the cytoarchitecture and function of the gastric mucosa against the severe damages provoked by ethanol intake. Ulcerated areas were very significantly reduced and the % of ulcer inhibition was the highest under OFI oil pretreatment. Mucus production was stimulated, gastric juice volume was reduced, and its pH was increased. Histopathological examination of H&E-stained biopsies collected from gastric mucosae from the different experimental groups confirmed the gastroprotective efficacy of OFI oil against ethanol-induced symptoms such as inflammation and damages like bleeding, erosions, lesions, necrosis, and ulcers. Furthermore, OFI oil treatment speeded-up the reduction of the surface of ethanol-induced ulcerated areas in a dose-dependent manner, leading to a time gain in the healing process. The healing rate reached 91% on day 2 and 99% on day 3, and a complete heal was attained at the fourth day under OFI oil treatment, while ulcer areas were still partially unhealed in all the other groups. The therapeutic effects of OFI oil against gastric ulcer could be mediated by its varied bioactive compounds that we have demonstrated in the analytical study. They could act synergistically or in a delayed manner to optimize the healing process through protective antioxidant properties, as well as an antagonism against histamine H2-receptors, a stimulation of the signaling pathways necessary for mucus and bicarbonate production, and reduction of inflammatory processes in the gastric mucosa. Additionally, OFI oil fatty acids (especially unsaturated) and triacylglycerols contribute to the reconstruction and the repair of the cell membrane lipid bilayer during the gastric ulcer healing process.
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Filaretova, Ludmila, Tatiana Podvigina, and Natalia Yarushkina. "Physiological and Pharmacological Effects of Glucocorticoids on the Gastrointestinal Tract." Current Pharmaceutical Design 26, no. 25 (August 4, 2020): 2962–70. http://dx.doi.org/10.2174/1381612826666200521142746.
Abstract:
The review considers the data on the physiological and pharmacological effects of glucocorticoids on the gastric mucosa and focuses on the gastroprotective role of stress-produced glucocorticoids as well as on the transformation of physiological gastroprotective effects of glucocorticoids to pathological proulcerogenic consequences. The results of experimental studies on the re-evaluation of the traditional notion that stress-produced glucocorticoids are ulcerogenic led us to the opposite conclusion suggested that these hormones play an important role in the maintenance of the gastric mucosal integrity. Exogenous glucocorticoids may exert both gastroprotective and proulcerogenic effects. Initially, gastroprotective effect of dexamethasone but not corticosterone, cortisol or prednisolone can be transformed into proulcerogenic one. The most significant factor for the transformation is the prolongation of its action rather the dose. Gastrointestinal injury can be accompanied by changes in somatic pain sensitivity and glucocorticoids contribute to these changes playing a physiological and pathological role.
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Waseem, Uzma, Syeda Rizwana Jafri, Sarah Khalid, Fauzia Qureshi, Nadia Majeed, and Ursula Akif. "Anti-inflammatory activity of acacia catechu-bark aqueous solution in aspirin induced gastric ulcer in rodents." International Journal Of Community Medicine And Public Health 8, no. 12 (November 24, 2021): 5649. http://dx.doi.org/10.18203/2394-6040.ijcmph20214551.
Abstract:
Background: Aspirin is amongst the most widely used drugs and has many adverse effects on gastric mucosa. Anti-inflammatory properties of Acacia catechu have been established already. Objective was to evaluate the histopathological changes induced by aspirin in the stomach of albino rats and to assess the protective effect of different doses of Acacia catechu.Methods: Experimental study Postgraduate Medical Institute, Lahore for 21 days. Forty-eight adult albino rats, both males and female, were divided into four groups A, B, C and D randomly; each comprising of 12 rats. Group A was control, group B was given aspirin 100 mg/kg and group C and D were given aspirin 100 mg/kg along with Acacia catechu 250 mg/kg and 500 mg/kg respectively by oral route. The rats from individual group were sacrificed on 3rd day, 7th day and 14th day and stomachs were examined under light microscope to observe the inflammatory cells infiltration.Results: Gross and microscopic findings on days 3, 7 and 14 were similar. Control groups A1, A2 and A3 showed normal healthy gastric mucosa and the least number of inflammatory cells. In group B, aspirin produced ulcerations and linear breaks; with highest inflammatory infiltrates. On microscopic examination, numerous inflammatory cells were noted. Group C and D rats had minimum ulcer index and fewer inflammatory cells.Conclusions: Acacia catechu has protective role against gastric injury by inhibiting inflammation.
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Ishikawa, T., B.-L. Zhu, and H. Maeda. "Effects of therapeutic agents on cellular respiration as an indication of metabolic activity." Human & Experimental Toxicology 25, no. 3 (March 2006): 135–40. http://dx.doi.org/10.1191/0960327106ht610oa.
Abstract:
Animal experiments are indispensable in the investigation of the toxicity of drugs on cells, but may not be preferred for ethical reasons and sensitivity. As an alternative procedure, we investigated the susceptibility of cells to drugs using the effect on cellular respiration as an indicator of cell activity (toxicity). The primary cultures (cell lines) used in this study included human fetal myocardial cells, skeletal muscle cells, nerve cells, hypophyseal cells, epithelial cells of gastric mucosa, lymphocytes, hepatocytes, pancreatic (exocrine) cells, renal tubular epithelial cells and fetal adrenal cortex cells, which were obtained from the American Type Culture Collection (ATCC). The drugs used were diazepam, haloperidol and levomepromazine maleate (psychoactive drugs), cisplatin and doxorubicin hydrochloride (anticancer agents). The cells were used at a density of 2–106 cells/2 mL of growth medium and, to test the susceptibility, each drug was prepared at a concentration of 10 g/mL. Experiment results indicated that, even with the same drug, sensitivity was markedly different depending on the cell lines. Cardiac muscle cells showed the strongest respiratory inhibition by Serenace and were least inhibited by Hirnamin. The highest sensitivity to Cercine was noted for neurons, while gastric mucosa cells had almost no sensitivity. Sensitivity to Serenace, which was expected to have a strong nerve action, was higher in myocardial cells instead. In the present study, we suggested the possibility of studying individual differences in drug sensitivity through investigation of toxicity in each organ as opposed to toxicity in the individual. In addition, Serenace, which was developed as a neurotopic agent, showed a higher toxicity in cardiac muscle cells than in neurons. This finding appeared noteworthy, not only for forensic toxicology, but also for clinical practice and drug development.
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Bibik, E. Yu, A. V. Myazina, K. A. Frolov, V. V. Dotsenko, and S. G. Krivokolysko. "Influence of new 1,4‑dihydrothiopyridine derivatives with analgesic activity on the gastric mucosa." Glavvrač (Chief Medical Officer), no. 7 (July 1, 2022): 9–11. http://dx.doi.org/10.33920/med-03-2207-01.
Abstract:
In clinical practice, such a side effect as gastrotoxicity can occur in patients taking NSAIDs with any route of administration. In this case, damage not only to the upper parts of the digestive tract, but also to the intestine as a whole is noted, since NSAID-induced enteropathy is manifested by a breach in the intestinal permeability with protein exudation and diapedesis of erythrocytes, as well as by the damage with the development of erosions, ulcers and life-threatening complications: bleeding, perforation, intestinal obstruction, the occurrence of circular structures [1]. The purpose of the study: to investigate the morphofunctional state of the stomach after exposure to non-steroidal anti-inflammatory drugs and new heterocyclic compounds synthesized by us with previously proven high analgesic activity in white rats.
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Paseban, Maryam, Saeed Niazmand, Mohammad Soukhtanloo, and Naser Tayyebi Meybodi. "The preventive effect of Nigella sativa seed on gastric ulcer induced by indomethacin in rat." Journal of Herbmed Pharmacology 9, no. 1 (January 1, 2020): 12–19. http://dx.doi.org/10.15171/jhp.2020.02.
Abstract:
Introduction: Nonsteroidal anti-inflammatory drugs (NSAIDs) are considered as one of the most administrated groups of medications worldwide. Due to the role of NSAIDs in inducing gastric ulceration, their clinical applications are still challenging. Nigella sativa seed is widely used as an herbal medication against gastrointestinal complications. The present experiment was carried out to investigate the impact of N. sativa seed hydro-alcoholic extract on gastric ulcer induced by indomethacin (IND) and to evaluate its possible mechanisms in rat. Methods: This study was performed on 48 male Wistar rats. Acute gastric ulceration was induced by IND (35 mg/kg). N. sativa seed extract (100, 200, 400 mg/kg) and ranitidine (50 mg/kg) were administered orally for five days before the induction ulcer. Ulcer index, gastric acid secretion, gastric mucus content, glutathione (GSH), malondialdehyde (MDA), total hexose, gastric juice protein content were determined on the fifth day. Results: The ulcer index in all groups of N. sativa seed was significantly lower than that of the IND group. N sativa seed considerably decreased MDA and protein content, but increased total thiol, total hexose, and mucus content compared to the IND group. N. sativa seed did not affect gastric acid secretion. Conclusion: These findings were indicative of the gastroprotective effect of N. sativa seed against the IND-induced ulcer, suggesting that it can mainly be exerted through the anti-oxidant activity of the extract as well as its role in stimulating gastric mucus secretion and increasing total hexose in the gastric mucosa.
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Frolova, A. A., T. S. Shindina, L. V. Maslovsky, M. L. Maksimov, E. B. Aleksandrova, and O. E. Kropova. "Mechanism of action of gastroprotective agent rebamipide." Glavvrač (Chief Medical Officer), no. 8 (July 25, 2022): 23–25. http://dx.doi.org/10.33920/med-03-2208-06.
Abstract:
Among the diseases of the digestive system, a significant place is occupied by acid-dependent diseases caused by excessive secretion of hydrochloric acid secreted by the parietal cells of the gastric mucosa. Due to their high prevalence and risk of complications, these pathologies represent a serious medical and social problem. Gastroprotective agents have a protective effect on the mucous membrane of the stomach and intestines. This group of medicines includes a range of drugs that differ in principle and mechanism of action, such as misoprostol, bismuth salts, as well as some herbal preparations, etc.
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Takeuchi, Kenichiro, Maki Ohishi, Keiko Endo, Kenichi Suzumura, Hitoshi Naraoka, Takeji Ohata, Jiro Seki, Yoichi Miyamae, Masashi Honma, and Tomoyoshi Soga. "Hydroxyproline, a Serum Biomarker Candidate for Gastric Ulcer in Rats: A Comparison Study of Metabolic Analysis of Gastric Ulcer Models Induced by Ethanol, Stress, and Aspirin." Biomarker Insights 9 (January 2014): BMI.S15918. http://dx.doi.org/10.4137/bmi.s15918.
Abstract:
Gastrointestinal symptoms are a common manifestation of adverse drug effects. Non-steroid anti-inflammatory drugs (NSAIDs) are widely prescribed drugs that induce the serious side effect of gastric mucosal ulceration. Biomarkers for these side effects have not been identified and ulcers are now only detectable by endoscopy. We previously identified five metabolites as biomarker candidates for NSAID-induced gastric ulcer using capillary electrophoresis–mass spectrometry (CE–MS)-based metabolomic analysis of serum and stomach from rats. Here, to clarify mechanism of changes and limitations of indications of biomarker candidates, we performed CE–MS-based metabolomic profiling in stomach and serum from rats with gastric ulcers induced by ethanol, stress, and aspirin. The results suggest that a decrease in hydroxyproline reflects the induction of gastric injury and may be useful in identifying gastric ulcer induced by multiple causes. While extrapolation to humans requires further study, hydroxyproline can be a new serum biomarker of gastric injury regardless of cause.
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Ye, Junhong, Jifu Li, and Ping Zhao. "The Silkworm Carboxypeptidase Inhibitor Prevents Gastric Cancer Cells’ Proliferation through the EGF/EGFR Signaling Pathway." International Journal of Molecular Sciences 24, no. 2 (January 5, 2023): 1078. http://dx.doi.org/10.3390/ijms24021078.
Abstract:
Gastric cancer is a common malignant tumor originating from the gastric mucosa epithelium. Studies have shown that bioactive substances such as antimicrobial peptides and cantharidin contained in a variety of insects can exert anti-cancer functions; when compared with chemotherapy drugs, these bioactive substances have less toxicity and reduced side effects. Here, we report the first Bombyx mori carboxypeptidase inhibitor that is specifically and highly expressed in silk glands, which can significantly prevent the proliferation of gastric cancer cells by inhibiting the MAPK/ERK pathway initiated by EGF/EGFR through the promotion of expression of the proto-oncogene c-Myc, thereby affecting the expression of related cyclins. Through molecular docking and virtual screening of silkworm carboxypeptidase inhibitors and epidermal growth factor receptors, we identified a polypeptide that overlapped with existing small-molecule inhibitors of the receptor. In the present work, we explore the medicinal potential and application of silkworm carboxypeptidase inhibitors to promote the development of anti-tumor drugs from insect-derived substances.