Induction Of Gastric Ulcer Research Articles

Changes in Heart Rate Variability with Induction of Gastric Ulcers in Adult Horses.

Gastric ulceration can be induced by athletic training and is a significant welfare concern. The objective of this study was to evaluate the effect of gastric ulcer induction on heart rate variability (HRV) in the horse. We hypothesized that induction of gastric ulcers would decrease HRV and increase low frequency fluctuations, consistent with increased sympathetic tone. A convenience sample of 8 horses in a larger study were enrolled. Horses were randomly assigned to receive water or 2 mg/kg omeprazole orally once daily for 28 days. Gastric ulcers were induced through intermittent feed withholding on days 21 to 28. Gastroscopy was performed and gastric ulcers were graded (0-IV) by three blinded reviewers on days 21 and 28. Continuous electrocardiograms were obtained for one hour at the start and end of ulcer induction. HRV was assessed in 1-hour recordings for time domain variables and 5 minute sections for frequency domain analysis. HRV and ulcer grade across treatments were compared by a mixed effect model, with treatment and time as fixed effects and horse as a random effect. Gastric ulcer grade increased with induction protocol (P < .0001) and decreased with omeprazole treatment (P=.0007). Omeprazole treatment increased R-R intervals (P=.01) and decreased ratio of low frequency/high frequency signal (P=.008) as compared to horses receiving water. This was attributable to decreasing low frequency fluctuations (P=.05). While limited by the small sample size (four horses/treatment), this study suggests that omeprazole treatment decreases heart rate, and LF/HF ratio during ulcer induction, consistent with a decrease in sympathetic tone.

Alterations in Hemostatic and Hematological Parameters after Gastric Ulcer Induction in Rats. Possible Role of IL-6 and TNF-α

Alterations in Hemostatic and Hematological Parameters after Gastric Ulcer Induction in Rats. Possible Role of IL-6 and TNF-α

Achillea millefolium Essential Oil Mitigates Peptic Ulcer in Rats through Nrf2/HO-1 Pathway.

Extreme ethanol ingestion is associated with developing gastric ulcers. Achillea millefolium (yarrow) is one of the most commonly used herbs with numerous proven pharmacological actions. The goal of the hereby investigation is to explore the gastroprotective action of yarrow essential oil against ethanol-induced gastric ulcers and to reveal the unexplored mechanisms. Rats were distributed into five groups (n = 6); the control group administered 10% Tween 20, orally, for two weeks; the ethanol group administered absolute ethanol (5 mL/kg) to prompt gastric ulcer on the last day of the experiment. Yarrow essential oil 100 or 200 mg/kg + ethanol groups pretreated with yarrow oil (100 or 200 mg/kg, respectively), orally, for two weeks prior to gastric ulcer induction by absolute ethanol. Lanso + ethanol group administered 20 mg/kg lansoprazole, orally, for two weeks prior to gastric ulcer induction by ethanol. Results of the current study showed that ethanol caused several macroscopic and microscopic alterations, amplified lipid peroxidation, pro-inflammatory cytokines, and apoptotic markers, as well as diminished PGE2, NO, and antioxidant enzyme activities. On the other hand, animals pretreated with yarrow essential oil exhibited fewer macroscopic and microscopic modifications, reduced ulcer surface, and increased Alcian blue binding capacity, pH, and pepsin activity. In addition, yarrow essential oil groups exhibited reduced pro-inflammatory cytokines, apoptotic markers, and MDA, restored the PGE2 and NO levels, and recovered the antioxidant enzyme activities. Ethanol escalated Nrf2 and HO-1 expressions, whereas pretreatment of yarrow essential oil caused further intensification in Nrf2 and HO-1. To conclude, the current study suggested yarrow essential oil as a gastroprotective agent against ethanol-induced gastric lesions. This gastroprotective effect could be related to the antioxidant, anti-inflammatory, and anti-apoptotic actions of the essential oil through the instigation of the Nrf2/HO-1 pathway.

Sonchus oleraceus L. Promotes Gastroprotection in Rodents via Antioxidant, Anti-Inflammatory, and Antisecretory Activities.

Sonchus oleraceus L. is an edible and medicinal plant used to treat stomachache and gastric ailments around the world. Thus, this study aimed to determine the gastroprotective mode of action of hydroalcoholic extract of S. oleraceus (HES). Mice were treated with HES before induction of gastric ulceration by ethanol/HCl. The area and histological appearance of ulcers were quantified, and mucus was measured histochemically. The effects of HES on inflammatory and oxidative markers were assessed in the ulcerated tissue. In addition, we investigated the gastric acid antisecretory activity of HES in pylorus-ligated rats. Chemical analyses of HES and its antioxidant activity were also performed in vitro. The HES (30 or 300 mg/kg) reduced the ulceration by 71.5 and 76.2%, respectively, compared with vehicle (p < 0.001), and the histological analysis confirmed the macroscopic results with elevation in mucin levels by 361.4 and 477.5%, respectively, compared with vehicle (p < 0.001). Moreover, the gastroprotection was accompanied by increases in GSH levels and in SOD, CAT, and GST activities; in parallel to a reduction in MPO activity and TNF levels. Furthermore, HES reduced the total acidity, and pepsin activity of the gastric juice of rats by 61 and 63%, respectively, compared to the vehicle. Phytochemical analysis indicated that luteolin-7-O-β-D-glucoside is the main active compound annotated in HES. Was also found that HES scavenged the DPPH radical with an IC50 of 15.41 μg/mL. In conclusion, the gastroprotective effects of HES involve reductions in oxidative stress and inflammatory injury, in conjunction with an increase in mucus layer and inhibition of gastric secretion. This study advances in elucidating the modes of the antiulcer potential of S. oleraceus and contributes to the prospection of new gastroprotective molecules.

Effect Of Plasmodium Berghei Parasitaemia On Laboratory Induced Gastric Ulcer In Mice

Background: Malaria is an important infection in Africa affecting all age groups although its severity depends on the relative immunity of the individual. Malaria has been found to have effects on the gastric mucosa, which include congestion with capillary stasis, necrosis, ulceration and haemorrhage. This study aimed at the effect of malaria parasitaemia on laboratory induced gastric ulcer in mice.Methods: Thirty-six mice divided into 6 groups thus: Group 1. no malaria parasite and ulcer (control); Group 2. Parasite without ulcer; Group 3. Parasite and ulcer; Group 4. Ulcer without parasite; Group 5. Parasite, ulcer and chloroquine treatment; and Grop 6. Parasite,ulcer and Artemether treatment. These were used for the study. The mice were parasitized with 20% innoculum of Plasmodium berghei and ulcer induced with 70% alcohol and pylorus ligation. Parameters such as degree of parasitization, ulcer diameter, gastricacidity and packed cell volume (PCV) were measured in the various groups and comparison made where necessary. The experimental part of the study took 18 days.Results: The severity of ulceration in the group with ulcer and parasite (11 ± 1.72 mm); and group with ulcer but no parasite (3.62 ± 1.6mm) was compared and was significant (p = 0.002). The groups with parasite showed gradual reduction in the packed cell volume (PCV) as the parasite load increased while the group without parasite showed increase in PCV over the time of study. The ulcer diameters in the groups treated with chloroquine (4.83 ± 2.48mm) and Artemether (5.00 ± 0.89) was not statistically significant (p = 0.889). The restoration of PCV was better for the treated group than the untreated group. The pH of the gastric content in the untreated group was lower than the treated groups. The parasite clearance by chloroquine and artemether was significant (p = 0.04) compared to the untreated groups.Conclusion: Malaria parasitaemia has a significant influence on gastric ulceration, PCV and to some extent gastric secretion. Chloroquine and artemether are sensitive drugs to Plasmodium berghei.

Moringa oleifera alcoholic extract protected stomach from bisphenol A–induced gastric ulcer in rats via its anti-oxidant and anti-inflammatory activities

This study evaluated the protective potentials of Moringa oleifera leaf alcoholic extract (MOLE) against bisphenol A (BPA)-induced stomach ulceration and inflammation in rats. Control rats received olive oil. Second group administered MOLE (200 mg/kg bwt) by oral gavage. Third group was given BPA (50 mg/ kg bwt) for 4 weeks. Fourth group administrated BPA and MOLE simultaneously. Fifth group was given MOLE for 4 weeks then administered BPA and MOLE for another 4 weeks. Bisphenol A induced gastric ulceration and decreased the volume of gastric juice, prostaglandin E2 (PGE2), reduced glutathione (GSH) and interleukin 10 (IL-10) contents, superoxide dismutase (SOD) activity, and proliferating cell nuclear antigen (PCNA) protein in stomach tissues, while increased the titratable acidity, malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) contents, and caspase-3 and NF‑κB proteins in stomach tissue. However, MOLE ameliorated BPA-induced gastric ulceration and significantly increased the volume of gastric juice, PGE2, GSH and IL-10 contents, SOD activity, and PCNA protein while significantly decreased titratable acidity, MDA, TNF-α and IL-6 contents, and of NF‑κB and caspase-3 proteins in gastric tissue. This study indicated that MOLE protected stomach against BPA-induced gastric injury via its anti-oxidant, anti-apoptotic, and anti-inflammatory activities.

Kombucha fermentation in blueberry (Vaccinium myrtillus) beverage and its in vivo gastroprotective effect: Preliminary study

Kombucha is a fermented beverage, usually made from green tea and/or black tea, obtained through the symbiotic growth of yeasts and bacteria with beneficial effects to health. This preliminary study developed and evaluated the protective effect of blueberry fermented and unfermented Kombucha beverages after induction of gastric ulcer in mice. We performed a physicochemical characterization of the beverages and after 15 days of intervention with the beverages, the Swiss mice were euthanized and biochemical analysis, lipid peroxidation and advanced oxidation protein products determination, and evaluation of gastrointestinal wound were performed. The results were evaluated after checking normality, by parametric or nonparametric tests, at 5% probability. The use of blueberry as an alternative substrate for fermentation of kombucha beverage was favorable in relation to the physico-chemical aspects, due to the increased phenolic compounds, tannins and anthocyanins contents in the fermented beverage. However, the fermentation caused smaller antioxidant activity when compared to the unfermented beverage. In relation to the gastroprotective effect of the fermented kombucha beverage, the biochemical parameters remained at normal levels, however, some animals showed gastric lesions in an expressive area. Further studies are needed to better understand the antioxidant potential of the blueberry fermented kombucha beverage and its gastroprotective effects.

Antiulcer activity of proanthocyanidins is mediated via suppression of oxidative, inflammatory, and apoptotic machineries.

Gastric ulcer (GU) is a lesion in the gastric mucosa associated with excessive oxidative damage, inflammatory response, apoptotic events, and irritation which may develop into cancer. However, medications commonly used in GU treatment cannot normalize gastric mucosa, while causing several adverse effects. Proanthocyanidins (PAs) are dietary flavonoids with numerous biological and pharmacological activities. In the current investigation, we studied the potential anti-ulcerative activity of PAs against acidified ethanol (HCl/ethanol)-caused gastric ulceration. Fifty male albino Wistar rats were allocated into five equal groups: control, HCl/ethanol (3mL/kg), lansoprazole (LPZ, 30mg/kg)+HCl/ethanol, and PAs (100 and 250mg/kg)+HCl/ethanol. LPZ and PAs were applied one week before gastric ulcer induction. PAs pretreatment notably reduced gastric mucosal macroscopic and microscopic pathological changes in a dose-dependent manner. Additionally, PAs activated the innate antioxidant molecules including glutathione and its derived antioxidants (glutathione peroxidase and glutathione reductase), along with superoxide dismutase and catalase, while attenuating pro-oxidant formation, including malondialdehyde and nitric oxide. Interestingly, PAs supplementation at a higher dose suppressed gastric inflammatory and apoptotic responses, as demonstrated by the reduced levels of interleukin-1β, interleukin-6, tumor necrosis factor alpha, high-mobility group box 1, cyclooxygenase 2, prostaglandin E2, nuclear factor kappa-B, Bcl-2-associated X protein, and caspase-3, while B cell lymphoma 2 was elevated. Hence, PAs could exhibit antiulcer activity by protecting gastric tissue from the development of oxidative damage, inflammatory responses, and apoptosis events associated with ulceration. PRACTICAL IMPLICATIONS: Gastric ulcer is a lesion in the gastric mucosal layer associated with excessive inflammatory response, apoptotic events, oxidative damage, and irritation, and may develop into cancer with about 5%-10% morbidity rate. However, medications commonly used in GU treatment cannot normalize gastric mucosa, while causing several adverse effects. Therefore, new therapeutic approaches are needed to treat or prevent gastric ulceration. Proanthocyanidins (PAs, condensed tannins) are dietary flavonoids found in abundance in different plant species, including their fruits, bark, and seeds. Due to their potent antioxidative activity, PAs have been applied to prevent or treat oxidative stress-related diseases, including cancer, as well as metabolic, neurodegenerative, cardiovascular, and inflammatory disorders. Here, we examine the potential therapeutic role of proanthocyanidins (PAs) against acidified ethanol-induced gastric ulcer in rats through evaluating oxidative challenge, inflammatory response, apoptotic events, and histopathological changes in the gastric tissue.

Olmesartan niosomes ameliorates the Indomethacin-induced gastric ulcer in rats: Insights on MAPK and Nrf2/HO-1 signaling pathway.

Gastric ulcer is a continuous worldwide threat that inquires protective agents. Olmesartan (OLM) has potent anti-oxidant and anti-inflammatory characters, yet having limited bioavailability. We targeted the gastro-protective potential and probable mechanism of OLM and its niosomal form against indomethacin (IND) induced-gastric ulcer in rats. we prepared OLM niosomes (OLM-NIO) with different surfactant: cholesterol molar ratios. We evaluated particle size, zeta-potential, polydispersity, and entrapment efficiency. In-vitro release study, Fourier transform infrared spectroscopy, differential scanning calorimetry, and transmission electron microscopy were performed for selected niosomes. In-vivo, we used oral Omeprazole (30mg/kg), OLM or OLM-NIO (10mg/kg) for 3days before IND (25mg/kg) ingestion. We assessed gastric lesions, oxidative and inflammatory markers. OLM-NIO prepared with span 60:cholesterol ratio (1:1) showed high entrapment efficiency 93 ± 2%, small particle size 159.3 ± 6.8nm, low polydispersity 0.229 ± 0.009, and high zeta-potential -35.3 ± 1.2mV, with sustained release mechanism by release data. In-vivo macroscopical and histological results showed gastro-protective effects of OLM pretreatment, which improved oxidative stress parameters and enhanced the gastric mucosal cyclooxygenase-1 (COX-1) and prostaglandin E2 (PGE2) contents. OLM pretreatment suppressed interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) contents and translocation of p38 mitogen-activated protein kinase (p38-MAPK). Besides, OLM substantially promoted the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) protective pathway. OLM-NIO furtherly improved all previous outcomes. We explored OLM anti-ulcerative effects, implicating oxidative stress and inflammation improvement, mediated by the Nrf2/HO-1 signaling pathway and p38-MAPK translocation. Meanwhile, the more bioavailable OLM-NIO achieved better gastro-protective effects compared to conventional OLM form.

Malvidin Protects against and Repairs Peptic Ulcers in Mice by Alleviating Oxidative Stress and Inflammation.

Peptic ulcer episodes cause damage to the stomach and intestine, with inflammatory cell infiltration and oxidative stress as the main players. In this study, we investigated the potential of anthocyanidin malvidin for preventive and curative peptic ulcer treatment. The anthocyanidin effects were examined in gastric ulcer mouse models induced by ethanol, non-steroidal anti-inflammatory drugs (NSAIDs), ischemia-reperfusion (IR), acetic acid and duodenal ulcer induced by polypharmacy. Expression levels of oxidative and inflammatory genes were measured to investigate the mechanism of anthocyanin activity. At a dose of 5 mg·kg−1, Malvidin prevented gastric ulcer induction by ethanol, NSAID and repaired the tissue after 6 days of IR. Moreover, the anthocyanidin accelerated the healing of acetic acid-induced ulcer, increased the gene expression of EGF and COX-1, and downregulated MMP-9. Anthocyanin treatment mitigated the effect of polypharmacy on inflammation and oxidative stress observed in the intestine. Additionally, the compound downregulated cytokine expression and TLR4 and upregulated HMOX-1 and IL-10, exhibiting protective activity in the mouse gut. Malvidin thus prevented gastric and duodenal ulcers due to prominent anti-inflammatory and antioxidative effects on the gastrointestinal tract that were related to gene expression modulation and an increase in endogenous defense mechanisms.

(-)-Carveol Prevents Gastric Ulcers via Cytoprotective, Antioxidant, Antisecretory and Immunoregulatory Mechanisms in Animal Models.

Background: (-)-Carveol (p-Mentha-6,8-dien-2-ol) is a monocyclic monoterpenic alcohol, present in essential oils of plant species such as Cymbopogon giganteus, Illicium pachyphyllum and in spices such as Carum carvi (cumin). Pharmacological studies report its antitumor, antimicrobial, neuroprotective, vasorelaxant, antioxidant and anti-inflammatory activity.Hypothesis/Purpose: The objective of this study was to evaluate the acute non-clinical oral toxicity, gastroprotective activity of monoterpene (-)-Carveol in animal models and the related mechanisms of action.Methods: Acute toxicity was assessed according to OECD guide 423 in mice. Ethanol, stress, NSAIDs and pylorus ligation-induced gastric ulcer models were used to investigate antiulcer properties. The related mechanisms of action were using the ethanol-gastric lesions protocol.Results: (-)-Carveol has low toxicity, with a lethal dose 50% (LD50) equal to or greater than 2,500 mg/kg according to OECD guide nº 423. In all gastric ulcer induction methods evaluated, (-)-Carveol (25, 50, 100 and 200 mg/kg, p.o.) significantly reduced the ulcerative lesion in comparison with the respective control groups. To investigate the mechanisms involved in the gastroprotective activity, the antisecretory or neutralizing of gastric secretion, cytoprotective, antioxidant and immunoregulatory effects were evaluated. In the experimental protocol of pylorus ligation-induced gastric ulcer, (-)-Carveol (100 mg/kg) reduced (p < 0.001) the volume of gastric secretion in both routes (oral and intraduodenal). The previous administration of blockers NEM (sulfhydryl groups blocker), L-NAME (nitric oxide synthesis inhibitor), glibenclamide (KATP channel blocker) and indomethacin (cyclo-oxygenase inhibitor), significantly reduced the gastroprotection exercised by (-)-Carveol, suggesting the participation of these pathways in its gastroprotective activity. In addition, treatment with (-)-Carveol (100 mg/kg) increased (p < 0.001) mucus adhered to the gastric wall. Treatment also increased (p < 0.001) levels of reduced glutathione (GSH), superoxide dismutase (SOD) and interleukin-10 (IL-10). It also reduced (p < 0.001) malondialdehyde (MDA), myeloperoxidase (MPO), interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) levels.Conclusion: Thus, it is possible to infer that (-)-Carveol presents gastroprotective activity related to antisecretory, cytoprotective, antioxidant and immunomodulatory mechanisms.

Comparative Study of the Efficacy of Prebiotics and Probiotics as Dietary Supplements in Rats with Gastric Ulcer

Gastric ulcer is considered as main problem of gastrointestinal disease, presenting one of the most important health issues in all societies. This comparative study designed to explore the anti-ulcerogenic role of probiotics and prebiotics and to evaluate the most potent effect against gastric ulcer. Sixty rats were distributed into 6 groups : G1 Healthy control; G2 gastric ulcer (GU), ulcer was induced by four oral doses of Aspirin 200 mg/kg b.w./week ;G3 Prebiotics (PreB) administered orally group ( 0.5 g/day); G4 Probiotics (ProB) administered orally group ( 0.5 mg/day); G5 Prebiotics (Therapeutic): prebiotics was administered orally at dose ( 0.5g/day) for 30 days after induction of gastric ulcer (GU+PreB); G6 Probiotics (Therapeutic): probiotics was administered orally at dose ( 0.5mg/day) for 30 days after induction of gastric ulcer (GU+ProB). Oxidative stress parameters and inflammatory markers were measured. Results revealed that: aspirin caused gastric ulcer associated with increased MDA, TNF-α, IL-6, and IL-10 and decreased gastroprotective mediators SOD, GSH, CAT, and PGE2compared with control rats. Treatment with prebiotics or probiotics efficiently reduces gastric injury, oxidative stress and proinflammatory cytokines. Comparing treatment groups showed that, Probiotics as a therapeutic group was the most potent demonstrated a hopeful role against gastric ulcer.

Taxifolin and gastro-adhesive microparticles containing taxifolin promotes gastric healing in vivo, inhibits Helicobacter pylori in vitro and proton pump reversibly in silico

Taxifolin (3,5,7,3,4-pentahydroxy flavanone or dihydroquercetin, Tax) was identified as a gastroprotective compound and a gastroadhesive formulation was recently developed to prolong its residence time and release in the stomach. So, the gastric healing effectiveness of Tax and gastro-mucoadhesive microparticles containing Tax (MPTax) against the acetic acid induced-gastric ulcer in rats was investigated in this study. Moreover, the interactions between Tax and H+/K+-ATPase were investigated in silico, and its anti- H. pylori activity was determined in vitro. The oral treatment with MPTax (81.37 mg/kg, containing 12.29% of Tax) twice a day for seven days reduced the ulcer area by 63%, compared to vehicle-treated group (Veh: 91.9 ± 10.3 mm2). Tax (10 mg/kg, p.o) reduced the ulcer by 40% but with a p = 0.07 versus Veh group. Histological analysis confirmed these effects. Tax and MPTax increased the gastric mucin amount, reduced the myeloperoxidase activity, and increased the glutathione reduced content at ulcer site. However, only MPTax decreased the lipoperoxide accumulation at ulcer site. Besides, Tax and MPTax normalize the catalase and glutathione S-transferase activity. Tax showed reversible interaction with H+/K+-ATPase in silico and its anti-H. pylori effects was confirmed (MIC = 625 μg/mL). These results suggest that the antiulcer property of Tax involves the strengthening of the gastric protective factors in parallel to its inhibitory interaction with H+/K+-ATPase and H. pylori. Considering that ulcer healing action displayed by Tax was favored by gastroadhesive microparticles, this approach seems to be promising for its oral delivery to treat acid-peptic diseases.

Evaluation of the effect of hydroalcoholic and flavonoid-enriched extracts of Dracocephalum kotschyi on indomethacin-induced gastric ulcer in rats.

Background and purpose:Dracocephalum kotschyi (Zaringiah) is a fragrant wild medicinal plant found in Iran. Traditionally, it is used for the treatment of rheumatism, asthma, and gastrointestinal ailments. So far no investigation has been done on the beneficial or side effects of D. kotschyi on peptic ulcer. Therefore, this research was performed to find out whether D. kotschyi extract would induce peptic ulcer or could alleviate existing peptic ulcer.Experimental approach:Effect of hydroalcoholic (DKHE) and flavonoid extracts (DKFE) of D. kotschyi were determined in normal or indomethacin-induced gastric ulcer rats (n = 6) and compared with the vehicle and ranitidine treated controls. All the treatments were carried out orally and 24 h later the stomach mucus was visually examined for peptic ulcers. A section of the stomach was taken for microscopic histopathological examinations while another section of the stomach was used for measurement of myeloperoxidase (MPO) and malondialdehyde (MDA) activities.Findings/Results:Oral administration of the DKHE and DKFE alone, did not cause any sign of gastric ulcer induction. The D. kotschyi extracts not only didn’t aggravate the induced ulcer but also significantly prevented the severity of gastric ulcer induction by indomethacin. In addition, DKHE and DKFE inhibited MPO (up to 58.2%) and MDA (up to 44.2%) activities indicating their anti-inflammatory and antioxidant potential action on the stomach-induced ulcer.Conclusion and implication:Usage of D. kotschyi extracts is not associated with gastric ulcer induction and its co-administration with NSAIDs would be beneficial for controlling both the inflammation and preventing gastric ulcer in diseases such as rheumatism.

The intervention of tert-butylhydroquinone protects ethanol-induced gastric ulcer in type II diabetic rats: the role of Nrf2 pathway.

Ethanol consumption increases the prevalence of gastric ulcer (GU) in rats with type II diabetes (T2D). Induction of GU by absolute ethanol (5mL/kg or 3.94g/kg) in the animal model resembles human ulcer characteristics. The aim was to investigate the role of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in the treatment of GU in diabetic condition. The rats were exposed to absolute ethanol 1 h before sacrifice and T2D was induced by combined exposure of high-fat diet and low dose streptozotocin. Pretreatment of tert-butylhydroquinone (tBHQ) (25 and 50mg/kg), metformin (500mg/kg), and omeprazole (20mg/kg) were given once daily for last three consecutive weeks. In ethanol-exposed diabetic rats, pretreatment with tBHQ, omeprazole, and metformin reduced gastric mucosal lesion, ulcer index, histological alterations, malondialdehyde level, and apoptosis. Furthermore, the intervention of tBHQ, omeprazole, and metformin improved the integrity of the stomach mucosa, glutathione, gastric pH, collagen, and goblet cells. tBHQ treatment improved ethanol-induced alterations of Nrf2, catalase, heat shock protein 70 (HSP70), NF-κB, and endothelin-1 expressions in diabetic rats. In diabetic conditions, the incidence of GU is increased due to elevated levels of reactive oxygen species, inflammatory mediators, depleted levels of cellular antioxidants, and altered gastric parameters. The tBHQ intervention could be a rational strategy to protect these changes.

The Possible Protective Effect of Platelet Rich Plasma on Aspirin Induced Gastric Ulcer in Adult Male Albino Rat

Background: High morbidity and mortality due to gastric ulcer made its management is a medical challenge. Platelet rich plasma (PRP) had been used for treatment of skin ulcers, some hair and bone problems as PRP contains many growth factors which make it suitable for management of gastric ulcer.Objectives: The current work was aimed to study the protective role of PRP on gastric ulcer induced by aspirin. Materials and Methods: Forty adult male albino rats were divided into four groups. Group I; sham control, group II received PRP, group III received aspirin for induction of gastric ulcer and group IV was provided with PRP then received aspirin. All rats were sacrificed then the fundic mucosa was processed for light and scanning electron microscopic study. Paraffin sections were stained by hematoxylin and eosin, mallory trichrome and combined periodic acid Schiff (PAS) and alcian blue (AB) stains. Immunohistochemical staining for iNOS and EGFR were also performed. Results: Aspirin had induced mucosal destruction in the form of ulceration, epithelial surface desquamation, hemorrhage, vacuolation and inflammatory cellular infiltration. Scanning electron microscopic examination of aspirin group showed decreased mucus, widening of gastric pits and cavitation of mucosal folds. PRP produced a great preservation of gastric structure in protected group (IV). Conclusion: It could be concluded that aspirin caused ulcerating changes in gastric mucosa and PRP had ameliorating effects on these changes.

The Possible Protective Effect of Platelet Rich Plasma on Aspirin Induced Gastric Ulcer in Adult Male Albino Rat

Background: High morbidity and mortality due to gastric ulcer made its management is a medical challenge. Platelet rich plasma (PRP) had been used for treatment of skin ulcers, some hair and bone problems as PRP contains many growth factors which make it suitable for management of gastric ulcer.Objectives: The current work was aimed to study the protective role of PRP on gastric ulcer induced by aspirin. Materials and Methods: Forty adult male albino rats were divided into four groups. Group I; sham control, group II received PRP, group III received aspirin for induction of gastric ulcer and group IV was provided with PRP then received aspirin. All rats were sacrificed then the fundic mucosa was processed for light and scanning electron microscopic study. Paraffin sections were stained by hematoxylin and eosin, mallory trichrome and combined periodic acid Schiff (PAS) and alcian blue (AB) stains. Immunohistochemical staining for iNOS and EGFR were also performed. Results: Aspirin had induced mucosal destruction in the form of ulceration, epithelial surface desquamation, hemorrhage, vacuolation and inflammatory cellular infiltration. Scanning electron microscopic examination of aspirin group showed decreased mucus, widening of gastric pits and cavitation of mucosal folds. PRP produced a great preservation of gastric structure in protected group (IV). Conclusion: It could be concluded that aspirin caused ulcerating changes in gastric mucosa and PRP had ameliorating effects on these changes.

Involvement of nitric oxide pathway in the anti-inflammatory effect of modafinil on indomethacin-, stress-, and ethanol -induced gastric mucosal injury in rat

Gastric ulcer is a prevalent disease with various etiologies, including non-steroidal anti-inflammatory drugs (NSAIDs), stress conditions, and alcohol, resulting in an inflammatory condition in the gastric mucosa. The aim of this study was to explore the protective effects of modafinil on gastric erosions induced by indomethacin, water-immersion stress, and alcohol in rats and to evaluate the role of nitric oxide (NO) pathway. Animals were allocated to the three experimental models of gastric ulcer – indomethacin (30 mg/kg PO), water-immersion stress, and ethanol (5 ml/kg PO). Induction of gastric ulcer in all models caused an increase in J-score (macroscopic assessment), biochemical markers, including tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and myeloperoxidase (MPO), and microscopic destructions. Administration of modafinil (50 and 100 mg/kg i. p) significantly improved J-score in the indomethacin (P < 0.05) and stress models (P < 0.001). Moreover, the level of TNF-α IL-1β, and MPO was deceased after modafinil administration (P < 0.001). However, modafinil did not have any effects on gastric injury induced by ethanol. In addition, co-administration of L-NAME (a non-specific NO synthase inhibitor) and aminoguanidine (an inducible NO synthase inhibitor) with modafinil significantly neutralized the gastroprotective effect of modafinil in the indomethacin and water-immersion stress groups (P < 0.05, and P < 0.01; respectively), while 7-nitroindazole (a neuronal NO synthase inhibitor) did not show such reversing effects. In conclusion, modafinil possesses gastroprotective effects on the gastric lesions induced by indomethacin and stress, which are probably mediated via the inflammation inhibition and NO pathway modulation.

Evaluation of Influence of Archachatina marginata Mucin on the Body Weight and Some Gastric Secretions of Wistar Rats Induced with Gastric Ulcer

The aim of this study was to evaluate the influence of A. marginata mucin on the gastric secretions and body weight of wistar rats induced with gastric ulcer. Thirty (30) adult male wistar rats were divided into six groups of five rats each. Group I (normal control) was administered with 2ml/kg distilled water, while Groups II III, IV and V were induced with ulceration via oral administration of 120mg/kg indomethacin. After ulceration had been confirmed successfully induced, while Group II was left untreated with mucin, III, IV and V were treated with 200mg/kg, 400mg/kg and 800mgl/kg mucin respectively. Meanwhile, Group VI was administered with 20mg/kg omeprazole (standard drug). Body weight of rats was determined after induction (initial) and after treatment (final). The values recorded for free acidity (FA), total acidity (TA), pepsin activity (PA) and acid output (AO) for the untreated ulcer rats (Group II) were significantly high (63.20±7.66mEq/L), (91.40±6.34mEq/L), (1.63±0.09μEq/L/4hr) and (0.43±0.04μg/ml) respectively. However, significant reduction in the aforementioned parameters was established with mucin treatment in a dose dependent manner, such that Group V administered with 800mg/kg manifested the lowest level of FA (47.40±7.19 mEq/L), TA (72.00±6.36), PA (1.39±0.07 μg/ml) and AO (0.16±0.05 μg/ml) which was not significantly different from the values recorded for Group VI treated with the standard drug (omeprazole).The values recorded on the body weight of Group II reduced with the induction of gastric ulcer. However, a dose dependent increase was observed in all treated groups. In conclusion, through this study, it has been established that A. marginata mucin could be explored for the development of anti-ulcer therapy.

Effectiveness of neem (Azadirachta indica a.juss) bark extract as a gastroprotektor

Background: Gastric ulcer is a digestive problem that has a high prevalence rate, peptic ulcer can cause complications such as bleeding in the gastrointestinal tract, perforation, recurrence, cancer and even death. The neem stem bark extract has a compound that can be a gastroprotective activity so that it can reduce the number of gastric ulcer and gastric acid levels. Gastroprotective effects of neem bark extract in combination have been widely studied can reduce gastric ulcer, but no one has examined the extract of neem bark as a single gastroprotector. Objective: This study aims to determine the dose of extract that can prove the extract of neem stem bark can inhibit the ulcer index by macroscopic observation and microscopic images of in rats Methods: This research is a purely experimental study carried out in July – September 2019. The neem stem bark extract was given to Wistar male white rats with various dosages for seven days orally, after 24 hours of fasting, induced gastric ulcer with ibuprofen 400 mg/kg. Mice were dissected to activate the ulcer index after 8 hours of induction of gastric ulcer. Result: The ulcus index of negative group (ibuprofen), positive group (ranidin), and extracts of mimba rods 250, 500, 1000, and 2000 CMG/kgBB in a row were 7.13, 16.76, 7.41, 2.32, and 2.00 (p= 0.034). Microscopic observations suggest a much better picture of histology after this extract. Conclusion: The extract of a mimba bark has gastroprotective activity at 2,000 mg/kgBB.