Gastric Ulcer Area Research Articles

The Gastroprotective Effect of Sicyos angulatus Against Hydrochloric Acid/Ethanol-Induced Acute Gastritis and Gastric Ulcer in Mice.

Gastritis and gastric ulcers are common gastric diseases that are caused by infection, drugs, alcohol consumption, or stress. These conditions lead to increased inflammatory cytokines and recruitment of leukocytes, which damage the stomach mucosa and exacerbate disease severity. Sicyos angulatus (SA), an annual vine in the Cucurbitaceae family, is known to have an anti-inflammatory effect, but its efficacy for preventing gastritis and gastric ulcers has not yet been evaluated. In the present study, we investigated the gastroprotective effect of SA using a hydrochloric acid/ethanol-induced gastric mucosal injury mouse model and lipopolysaccharide (LPS)-stimulated KATO III cells. Macroscopic analysis revealed a reduction in gastric ulcer area. Similarly, histopathological analysis showed a dose-dependent decrease in gastric mucosal injury, with significant improvement at 750 mg/kg of SA treatment. Gene expressions of inflammatory cytokines, chemokines, and adhesion molecule were reduced in the SA-administered group. Immunohistochemical staining indicated that SA significantly decreased neutrophil infiltration in the lamina propria and epithelium of the stomach. Kaempferol, a major bioactive flavonoid of SA, also improved gastric injury by reducing macroscopic and microscopic lesions, inflammatory mediator gene expression, and neutrophil infiltration. Furthermore, both SA and kaempferol downregulated LPS-mediated increases in inflammatory cytokines and chemokines following inhibition of p38 and c-Jun N-terminal kinase (JNK) phosphorylation in KATO III cells. These results suggest that SA can ameliorate gastric mucosal injury by inhibiting the recruitment of inflammatory cells, particularly neutrophils, and by suppressing p38 and JNK phosphorylation.

The Gastroprotective Effects of Anisomeles indica against Ethanol-Induced Gastric Ulcer through the Induction of IκB-α and the Inhibition of NF-κB Expression.

Anisomeles indica (L.) Kuntze is a traditional herb with multiple medicinal properties and with potential for preventing or treating various diseases. Acteoside, one of the active ingredients in A. indica, is prepared into commercially available products of A. indica HP813 powder. In this study, the gastroprotective effects of A. indica HP813 powder were evaluated. Wistar rats were treated with A. indica HP813 powder at doses of 0, 207.5, 415, and 830 mg/kg body weight for 28 days. Then, gastric ulcers were induced by the oral administration of 70% ethanol (10 mL/kg body weight) on day 28. The rats were sacrificed at the end of the trial, and stomach tissues were collected. These stomach tissues were then used for macroscopic, microscopic, and immunohistochemical analyses. The results indicated that the area of gastric ulcer was 48.61%, 35.30%, and 27.16% in the ethanol-induced group, 415 mg/kg A. indica HP813 powder group, and 830 mg/kg A. indica HP813 powder group, respectively. In addition, the lesion scores were 2.9, 2.4, and 2.3 in the ethanol-induced group, 415 mg/kg A. indica HP813 powder group, and 830 mg/kg A. indica HP813 powder group, respectively. The immunochemical staining of the gastric tissue revealed that A. indica HP813 powder reduced the expressions of TNF-α and NF-κB proteins in the gastric tissue, which had been induced by ethanol. Finally, A. indica HP813 powder protected the gastric ulcer from ethanol damage through IκB-α induction. The present results demonstrated that A. indica HP813 powder has protective effects against ethanol-induced gastric ulcer.

Gastroprotective effect of SKM-Gelcocid suspension on indomethacin induced gastric ulcer in female Wistar rats

Background: Peptic ulcer causes painful ulcers or lesions in the stomach or duodenum. It is also known as a gastric ulcer, which is damage to the gastric wall or lower portion of the esophagus. In the allopathic system, many medications such as H2 receptor antagonists, and anti-H. pylori, proton pump inhibitors, and others with rapid therapeutic activities were utilized to treat peptic ulcers.Purpose: The main aim of this work is to report an in-vivo gastro protective investigation of Saminathapuram Karuppana Gounder Maeilanandhan- Gelcocid suspension (SKM-GS), an Ayurveda formulation, using indomethacin-induced gastric ulcer rats.Study Design and Methods: In the present study we have reported the gastroprotective effect of SKM-GS, an Ayurveda formulation. Indicators such as gastric ulcer area, ulcer index, gastric wall mucus, non-protein sulfhydryl groups (NP-SH), and anti-oxidant enzymes secreted by treatment with SKM-GS on Indomethacin-induced ulcers in female Wistar rats.Result: The results showed a significant (p>0.001) reduction in gastric ulcer area, ulcer index, and an increase in ulcer preventive index. It further revealed an increase in gastric wall mucus and NP-SH secretion. Treatment with SKM-GS showed decreased levels of malondialdehyde (MDA) levels and increased levels of glutathione (GSH) and glutathione peroxidase (GPx) enzymes in the indomethacin-induced gastric ulcer rats. Female Wistar rats when treated with 200 mg/kg and 400 mg/kg of SKM-GS identical to Lansoprazole (Lanso) showed an increase in gastroprotective activity in a dose-dependent manner.Conclusion: The SKM-GS's gastro-protective properties were similar to the well-known anti-ulcer, Lansoprazole. These effects may be due to antioxidant activity.

Anti-oxidative stress and gastroprotective effect of Tri-Tharn-Thip tea against ethanol-induced gastric ulcer in rats

BackgroundTri-Tharn-Thip, a traditional Thai medicine, is a herbal formula used to promote milk production, wound healing, and gastric ulcer. However, no previous studies have reported its anti-gastric ulcer activity. This study aimed to evaluate the gastroprotective effects of Tri-Tharn-Thip tea (Tri-TTa) and explore its potential mechanisms of action by measuring the levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), mucin, and inducible nitric oxide synthase (iNOS). MethodsFor this purpose, 24 Wistars rats were divided into four groups. Group I, sham group, received distilled water; Group II, vehicle control group, received distilled water; Group III, positive control group, received omeprazole (20 mg/kg/d); and Group IV, Tri-TTa group, received Tri-TTa (500 mg/kg/d). The treatment protocol lasted 7 d, and all groups except for the sham group received 80 % ethanol on the last day, 4 h before scarification. The gastric tissue was removed; the ulcer area, ulcer score, and pH values were evaluated; and a histopathological examination of the gastric tissue was conducted. ROS, MDA, iNOS, SOD, CAT, and GSH levels were determined using ELISA. ResultsPretreatment with 500 mg/kg Tri-TTa significantly reduced the gastric ulcer area and ROS, MDA, and iNOS levels in rats with ethanol-induced gastric ulcers. Tri-TTa increased the levels of SOD, CAT, and GSH in gastric tissues. Tri-TTa administration also significantly increased mucin content. ConclusionTri-TTa exhibited gastroprotective properties that could be linked to decreased oxidative stress markers and elevated antioxidant enzyme levels.

Protective effect of Amauroderma rugosum ethanol extract and its primary bioactive compound, ergosterol, against acute gastric ulcers based on LXR-mediated gastric mucus secretions

BackgroundAmauroderma rugosum (Blume & T. Nees) Torrend (Ganodermataceae) is an edible mushroom with a wide range of medicinal values. Our previous publication demonstrated the therapeutic effects of the water extract of A. rugosum (WEA) against gastric ulcers. However, the protective effects of the ethanol extract of A. rugosum (EEA) on gastric mucosa and its major active constituents have not yet been elucidated. PurposeThis study aims to evaluate the gastroprotective effects and underlying mechanisms of EEA and its fat-soluble constituent, ergosterol, in acute gastric ulcers. Study design and methodSD rats were pre-treated with EEA (50, 100, and 200 mg/kg) or ergosterol (5, 10, and 20 mg/kg), and acute gastric ulcer models were constructed using ethanol, gastric mucus secretion inhibitor (indomethacin) or pyloric-ligation. The gastric ulcer area, histological structure alterations (H&E staining), and mucus secretion (AB-PAS staining) were recorded. Additionally, Q-PCR, western blotting, immunohistochemistry, ELISA, molecular docking, molecular dynamics simulations, MM-GBSA analysis, and surface plasmon resonance assay (SPR) were used to investigate the underlying mechanisms of the gastroprotective effect. ResultCompared with WEA, which primarily exerts its anti-ulcer effects by inhibiting inflammation, EEA containing fat-soluble molecules showed more potent gastroprotective effect through the promotion of gastric mucus secretion, as the anti-ulcer activity was partly blocked by indomethacin. Meanwhile, EEA exhibited anti-inflammatory effects by suppressing the production of IL-6, IL-1β, TNF-α, and NO, thereby inhibiting the MAPK pathway. Significantly, ergosterol (20 mg/kg), the bioactive water-insoluble compound in EEA, exhibited a gastroprotective effect comparable to that of lansoprazole (30 mg/kg). The promotion of gastric mucus secretion contributed to the effects of ergosterol, as indomethacin can completely block it. The upregulations of COX1-PGE2 and C-fos, an activator protein 1 (AP-1) transcription factor, were observed after the ergosterol treatment. Ergosterol acted as an LXRβ agonist via van der Waals binding and stabilizing the LXRβ protein without compromising its flexibility, thereby inducing the upregulation of AP-1 and COX-1. ConclusionEEA and its primary bioactive compound, ergosterol, exert anti-ulcer effects by promoting gastric mucus secretion through the LXRβ/C-fos/COX-1/PGE2 pathway.

Effect of Heparin on the Formation and Healing of Gastric Ulcers Induced by Acetic Acid Application on the Gastric Mucosa in Rats

The key factor in maintaining the integrity of the gastric mucosa is its normal blood supply, respectively, the use of drugs that improve it, including through a positive effect on the rheological properties of blood, is in demand for the treatment of gastric ulcer. These drugs include the anticoagulant heparin. The aim of the work is to study the effect of heparin on the formation and healing of gastric ulcers induced by the application of 60% acetic acid to the gastric mucosa in rats, while assessing the possible risk of bleeding. After application of acetic acid (day 0), the area of gastric ulcers was assessed on the 4th day (formation of the ulcers) and the 7th day (healing of the ulcers). To assess the effect on ulcer formation, heparin (1000 IU/kg/day, subcutaneously) was administered from days 0 to 3, and on the healing from days 4 to 6 after acid application. To check for possible bleeding under the influence of heparin, the level of hemoglobin in the blood was tested before acid application (basal), on the 4th and 7th days after application. The degree of bleeding was assessed based on the relative decrease in hemoglobin levels. The administration of heparin led to a decrease in the average area of ulcers both on the 4th and on the 7th day compared with that in control rats (heparin vehicle). In control rats, both on the 4th and on the 7th day, the hemoglobin level was reduced compared to the corresponding basal level. Heparin had no effect on the hemoglobin level at day 4, but potentiated the decrease in mean hemoglobin level at day 7, increasing the number of animals having a greater relative decrease in hemoglobin level compared to the corresponding control group. Thus, heparin may have a gastroprotective effect, manifested both in the weakening of the formation of an ulcer and in the acceleration of its healing, however, there is a risk of bleeding when the ulcer heals.

The protective effect of small black soybean (Vigna Mungo L.) polysaccharide on acetic acid-induced gastric ulcer in SD rats and its impact on gut microbiota and metabolites

Small black soybean (Vigna Mungo L.) is a kind of medicinal and edible plant with many potential health benefits for the human body. In this study, we investigated the potential anti-gastric ulcer effect of Vigna Mungo L. polysaccharides (VMP) using an acetic acid-induced gastric ulcer model in SD rats. The impact of VMP on the levels of antioxidant factors and growth factors in gastric tissue homogenate, serum metabolites, short-chain fatty acids (SCFAs) and gut microbiota in SD rats were analyzed. The results revealed that VMP exhibited a beneficial role in facilitating the healing process of gastric ulcers, specifically by reducing the area of gastric ulcers, increasing the levels of epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF), and improving oxidative stress status. Additionally, VMP modulated 20 potential serum biomarkers associated with gastric ulcers, thereby exerting a significant impact on multiple crucial metabolic pathways. Notably, VMP notably increased the levels of SCFAs, including acetic acid, propionic acid, i-butyric acid, n-butyric acid, i-valeric acid, n-valeric acid, in the colonic contents of rats with gastric ulcers. Furthermore, VMP effectively ameliorated gut microbiota dysbiosis in gastric ulcer rats by reducing the relative abundance of Firmicutes, Lachnospiraceae_NK4A136_group, Quinella and Lactobacillus, while increasing the relative abundance of Bacteroidota, Bacteroides, Oscillospiraceae_UCG-005, Muribaculaceae, Parasutterella and Ruminococcus. Correlation analysis showed that the relative abundance of Parasutterella and Lachnospiraceae_NK4A136_group were closely related to the changes of SCFAs and serum metabolites. These findings provide potential groundwork for the development of health products aimed at preventing and treating gastric ulcers.

Bovine lactoferrin inhibits resistant Helicobacter pylori in vitro and protects gastric mucosal injury in vivo

Helicobacter pylori (H. pylori) is associated with gastric mucosal injury, gastric ulcer and other gastrointestinal diseases. Resistance of H. pylori to antibiotics has become an obstacle to clinical eradication therapy. Bovine lactoferrin (bLF) has a broad spectrum of antibacterial effects, high safety and no side effects, which may be conductive to improving the dilemma of antibiotic resistance. We aimed to explore the bactericidal effect of bLF on resistant H. pylori and the protective effect on gastric mucosal injury. In vitro experiments demonstrated that bLF has obvious antibacterial effect on resistant H. pylori and synergistic antibacterial effect when combined with clarithromycin. The MIC and MBC of bLF against resistant H. pylori ranged from 1.25 to 5 mg mL−1. In vivo experiments showed that bLF could improve the degree of gastric mucosa injury, decrease the area of gastric ulcer. Results indicate that bLF has a wide clinical application prospect in medical field.

Gastro-protective Effect of Corn Diet against Indomethacin Induced Ulceration in Experimental Rats

Introduction: One of the most prevalent gastrointestinal ailments is gastric ulcer, which is caused by an imbalance between protective and aggressive factors. Zea mays Corn is a significant cereal crop containing natural phytochemical substances that are sources of nourishment. The methanolic extract of Corn, according to a previous study, lowers stomach acidity and inhibits the percentage of gastric ulceration with no knowledge on the mechanisms involved.
 Aim: This study investigated the underlying gastroprotective mechanisms of the Corn diet (ZD).
 Materials and Methods: Sixty male Wistar rats were used, randomly grouped into 6; 1(Normal control), 2(Ulcerated control), 3, 4, 5 (prefed with ZD -55%, 65%, 75%) and 6 (cimetidine- 25mg/kg) for 28 days. Gastric ulcer was induced by oral administration of indomethacin (40mg/kg) and animals were sacrificed after 4 hours. The stomach was excised and cleaned, it was then homogenized and centrifuged for biochemical assays.
 Results: There is a significant reduction in gastric ulcer area in all treated groups. Significant increase in gastric tissue mucin content and gastric mucosal SOD, NO and PGE2 levels and significant reduction in the MDA was observed in the ZD and cimetidine group. Histological evaluation showed tubular glands closely packed and separated from each other by laminar propia, however there is mild presence of inflammatory cells within the laminar propia in the ZD groups compared to ulcerated control group that showed moderate oedema with infiltration of inflammatory cells with mild vascular congestion in the mucosa. There is significant reduction in the macroscopic gastric mucosal lesions with percentage inhibition of 90%, 92%, 90% and 92% in the ZD (55%, 65% and 75%) and cimetidine group respectively.
 Conclusion: Results obtained from this study suggests that Zm diet may have anti-ulcerogenic properties by enhancing antioxidant enzymes as well as, nitric oxide and prostaglandin E2 mechanisms.

Evaluation of Acetic Acid-Induced Chronic Gastric Ulcer Healing by Propionyl-L-Carnitine Administration.

The aim of our study was to investigate the healing effect of propionyl-L-carnitine (PLC) on chronic gastric ulcers and its underlying mechanisms. This study included rats with gastric ulcers induced by applying serosal glacial acetic acid. These rats were then given either saline (vehicle) or PLC at doses of 60 and 120 mg/kg, administered orally 3 days after ulcer induction for 14 consecutive days. Our study found that treatment with PLC resulted in a reduction of the gastric ulcer area, a faster rate of ulcer healing, and stimulated mucosal restoration. Additionally, the treatment with PLC reduced the number of Iba-1+ M1 macrophages while increasing the number of galectin-3+ M2 macrophages, as well as desmin+ microvessels, and α-SMA+ myofibroblasts in the gastric ulcer bed. The mRNA expression of COX-2, eNOS, TGF-β1, VEGFA, and EGF in the ulcerated gastric mucosa was greater in the PLC-treated groups compared with the vehicle-treated rats. In conclusion, these findings suggest that PLC treatment may accelerate gastric ulcer healing by stimulating mucosal reconstruction, macrophage polarization, angiogenesis, and fibroblast proliferation, as well as fibroblast-myofibroblast transition. This process is associated with the upregulation of TGF-β1, VEGFA, and EGF, as well as modulation of the cyclooxygenase/nitric oxide synthase systems.

Involvement of sympathetic nerve activation in acupoint application induced improvement of gastric ulcer and motility in rats with gastric ulcer

To observe the effect of mustard oil application at "Liangmen" (ST21) on gastric ulcer (GU) and gastric motility and its association with the sympathetic nerve activity in rats with GU, so as to provide experimental basis for improvement of GU by acupoint application. Thirty-nine male SD rats were randomly divided into control (n=7), model, acupoint application (AA), medication (guanethidine, an adrenergic sympathetic antagonist) and AA+medication groups (n=8 in each of the latter 4 groups). The GU model was made by applying acetic acid-immersed filter paper onto the gastric antrum. For rats of the AA and AA+medication groups, 50% mustard oil was applied to left ST21 for 10 min, once a day, for 9 consecutive days. Rats of the medication and AA+medication groups received intraperitoneal injection of guanethidine solution (40 mg/kg) beginning from the modeling day on, once a day for 10 consecutive days. The rat's body weight of each group was recorded on the 0th, 1st, 3rd, 7th and 9th day. The intragastric peristaltic wave frequency and the myoelectrical activity (frequency of slow waves, and integration of fast waves) of the gastric smooth muscle were recorded by using PowerLab data acquisition system. The gastric ulcer area was measured after the rats were executed, and histopathological changes of gastric antrum tissues (histopathological score including epithelial cell injury, submucosal edema, hemorrhagic injury, inflammatory cell infiltration score) were observed after H.E. staining. Compared with the control group, the body weight ratio, frequency of gastric peristaltic waves and slow wave frequency of gastric smooth muscle were significantly decreased (P<0.001, P<0.05), while the ulcer area, total histopathological score, epithelial cell injury score, submucosal edema score, hemorrhagic injury score and inflammatory cell infiltration score were significantly increased in the model group (P<0.05, P<0.001). Relevant to the model group, the AA group had a significant increase in the body weight ratio, frequency of gastric peristaltic waves, slow wave frequency, integration of fast waves (P<0.05, P<0.001), and a considerable decrease in the ulcer area, total histopathological score, epithelial cell injury score, submucosal edema score, hemorrhagic injury score and inflammatory cell infiltration score (P<0.05, P<0.001), and the medication group has a significantly decrease in the frequency of gastric peristaltic waves (P<0.05). In comparison with the AA group, the body weight ratio, frequency of gastric peristaltic waves and slow wave frequency of gastric smooth muscle in both medication and AA+medication groups, and the integration of fast waves in the medication group were obviously lower (P<0.05, P<0.001, P<0.01), whereas the levels of ulcer area, total pathological score, submucosal edema score, hemorrhagic injury score and inflammatory cell infiltration score in both medication and AA+medication groups, and the epithelial cell injury score in medication group were significantly higher (P<0.05, P<0.001). Application of mustard oil at acupoint ST21 can effectively remit GU caused by acetic acid and regulate gastric rhythmic contraction, which was mediated by sympathetic nerve.

Bletilla striata Polysaccharide Nanoparticles Improved the Therapeutic Efficacy of Omeprazole on the Rat Gastric Ulcer Induced by Ethanol.

Gastric ulcers are a common clinical presentation affecting anyone, regardless of their age or gender. Nanoparticles (NPs) containing Bletilla striata polysaccharide (BSP) and omeprazole (OME) were investigated in the study for their therapeutic effect on gastric ulcers. Ethanol-induced gastric ulcers in rats (240 ± 30 g) were established. Our OME-BSP NPs were more stable than free OME in the acidic environment and can increase the absorption of OME in rat stomach, which was confirmed by in situ gastric absorption and distribution experiments. The extended blood circulation of OME-BSP NPs was also observed in rats with gastric ulcer. More importantly, OME-BSP NPs not only decreased the area of gastric ulcer and inhibited gastric acid secretion but also reversed gastric tissue damage and cell apoptosis, as revealed by HE and TUNEL staining. Subsequent SOD, MDA, PGE2, IL-6, and TNF-α tests further verified the superiority of OME-BSP NPs against rat gastric ulcer, which properly originated from superior antioxidant and anti-inflammatory effects. As a result, our OME-BSP NPs' drug delivery system improved the stability and absorption of OME in the rat stomach and achieved targeted treatment of gastric ulcers.

Anti-Ulcer Potentials of Aqueous Extract of Triticum aestivum on Delayed Healing of Experimentally Induced/Gastric Ulcer

Background: Ulcer reoccurrence and delay of healing caused by certain factors is now a major problem with the treatment of peptic ulcer. This study sought to unravel the role of Triticum aestivum in delayed ulcer healing in Wistar rats. Materials and Methods: Twenty five (25) Experimental animals (male Wistar rats) weighing 120g – 150g were randomly divided into five groups (N = 5) viz; I (Control), II (20% acetic acid ulceration + 2 mg/kg of indomethacin), III, IV, and V received 50 mg/kg, 100 mg/kg and 200 mg/kg of T. aestivum + 20% acetic acid ulceration + 2 mg/kg of indomethacin. Ulcer was induced by serosa application of 20% acetic acid and was delayed by subcutaneous administration of 2 mg/kg of indomethacin for 14 days. Results: Findings from this study showed that the relative body weight changes decreased substantially in delayed untreated group juxtaposed to control which was improved in T. aestivum extract (TAE) groups. Total gastric acidity, ulcer area, and relative stomach weight were substantially (P &lt; 0.05) increased in delayed ulcer group juxtaposed to control group. These changes were substantially reversed in TAE-treated groups. A substantial decrease was observed in the catalase level and expression of nitric oxide accompanied by an increase in malondialdehyde was noted in delayed ulcer group juxtaposed to control which were ameliorated in all TAE treated groups. Histological and macroscopic evaluations revealed that there was a substantial decrease in inflammation and erosion of the gastric mucosa in groups treated with T. aestivum juxtaposed to delayed ulcer group. Conclusion: It can thus be said that aqueous extract of T. aestivum attenuates delayed gastric ulcer healing due to antioxidants and anti-inflammatory properties. The highest concentration (200 mg/kg) in this proved to be the most beneficial.

Mechanisms of Dendrobium officinale polysaccharides in repairing gastric mucosal injuries based on mitogen-activated protein kinases (MAPK) signaling pathway

ABSTRACT The present study aimed to investigate the protective effects and molecular mechanisms of Dendrobium officinale polysaccharides on gastric mucosal injuries. Following one week of continuous intragastric administration, a gastric mucosal injury model was established using intragastric administration of anhydrous ethanol. The area of gastric ulcer was measured, the contents of interleukin- 6 (IL-6), epidermal growth factor receptor (EGFR), and thyroid transcription factor 1 (TFF-1) in serum were detected by enzyme linked immunosorbent assay (ELISA), and the expressions of EGFR, TFF-1, IL-6, Raf-2, MAP kinase kinase 1 (MEK1), MEK2, and ERK1 in the gastric tissue were determined utilizing qPCR, Western blotting and immunohistochemistry. Simultaneously, Dendrobium officinale polysaccharides and anhydrous ethanol were added to the gastric mucosal cells (GES1) cultured in vitro, and the protective effects of Dendrobium officinale polysaccharides on cell viability was detected using Cell Counting Kit (CCK)-8. The addition of Dendrobium officinale polysaccharides markedly improved the gastric epithelial defect, inflammatory cell infiltration, and redness and swelling stemmed from gastric mucosal injuries and greatly reduced the area of gastric ulcer. The inhibition rates of gastric ulcer were 48.12 ± 2.98, 42.95 ± 1.52, and 27.96 ± 2.05% in the high, medium, and low concentration Dendrobium officinale polysaccharide groups, respectively. Dendrobium officinale polysaccharides could increase the expressions of EGFR and TFF-1 and decrease the expressions of IL-6, Raf-2, MEK1, MEK2, and ERK1. Dendrobium officinale polysaccharides could reduce the level of inflammatory factors and protect gastric mucosa by inhibiting the expression of MAPK pathway genes and proteins.

Gastroprotective Effects of the Aqueous Extract from Taraxacum officinale in Rats Using Ultrasound, Histology, and Biochemical Analysis.

Taraxacum officinale F.H. Wigg. belonging to the family Asteraceae is an edible medicinal plant distributed worldwide. This study aimed to determine the gastroprotective effects of aqueous extract of T. officinale (AETo) in rats using ultrasound, histological, and biochemical analyses. In this study, gastric ulceration was induced by ethanol or piroxicam. Rats were then treated with AETo (3, 30, or 300 mg/kg). The area and histological appearance of gastric ulcers were quantified, and histochemical analysis was performed. The activity of AETo on inflammatory and oxidative stress markers was assessed in the ulcerated tissue. In addition, we investigated the thickness of the gastric wall using the ultrasound technique. Moreover, chemical analyses of AETo were performed. In rats with ethanol- or piroxicam-induced ulcers, AETo reduced the ulceration area, elevated mucin level, and the gastroprotective effect was confirmed by histological analysis. The gastroprotective effect was accompanied by increased activities of SOD, CAT, and GST, as well as an increase in GSH level and reduction in MPO activity. Furthermore, AETo reduced the thickness of the gastric wall in rats. Phytochemical analysis of AETo indicated phenolic acids and flavonoids as the main active compounds. In conclusion, the gastroprotective effect of AETo involves reduction in oxidative stress and inflammatory injury and increase in mucin content. This study advances in the elucidation of mechanisms of gastric protection of T. officinale, contributes to the prospection of new molecules gastroprotective, and proposes the ultrasonographic analyses as a new gastroprotective assessment tool in preclinical studies.

Gastroprotective action of the ethanol extract of Leonurus sibiricus L. (Lamiaceae) in mice

Ethnopharmacological relevanceLeonurus sibiricus L. (Lamiaceae) is a medicinal plant known in Brazil as “rubim” or “erva de macaé”. It is used for various purposes, including stomach disorders. Aim of the studyTo evaluate the effect of the ethanol extract of the aerial parts of L. sibiricus (EELs) in models of gastric damage in mice. Material and methodsThe effect of EELs (50, 100 and 300 mg/kg, p.o., 1 h before induction) was tested on acidified ethanol (ACEt)-induced gastric ulcers. Additionally, we tested the effect of EELs (by intraduodenal administration) in the pylorus ligation (PL) model. ResultsPretreatment with EELs, at 300 mg/kg, but not 50 and 100 mg/kg, reduced the relative area of gastric ulcers induced by ACEt (p < 0.01) and lipoperoxidation (p < 0.001), and increased the sulfhydryl content (p < 0.01) in the stomach in comparison with the vehicle group. Pretreatment with N-ethylmaleimide (a blocker of non-protein sulfhydryl groups, 10 mg/kg, i.p.) or glibenclamide (a KATP channel blocker, 10 mg/kg, i.p.) inhibited the gastroprotective response caused by EELs (300 mg/kg; p < 0.001), but there were no alterations due to pretreatments with inhibitors of the synthesis of prostaglandins (indomethacin, 10 mg/kg), nitric oxide (L-NAME, 70 mg/kg) or hydrogen sulfide (DL-propargylglycine, 10 mg/kg). Treatment with EELs (300 mg/kg) reduced mucus production (p < 0.001) and the volume of gastric secretion (p < 0.001) after PL without affecting gastric acidity or pH. ConclusionsThese results provide evidence that EELs exerts gastroprotective action in mice, with the participation of oxidative stress and mediation of NP-SH, KATP channels and mucus production.

Protective Effect of Pomegranate Peel Powder Against Gastric Ulcer in Rats

Gastric ulcer is a serious health problem that affects more than 10% of the World's population. Aspirin is the most common drug causes gastric ulcer also, most of the ulcer drugs have harmful side effects, so studies have focused on finding an alternative natural solution. This work provides a natural solution to protect the gut against ulcers, especially aspirin, by using a diet supplemented with pomegranate peel powder in rats. Levels of active components in pomegranate peel powder were detected using the certified methods. For the biological evaluation, 21 male rats (weight, 140-170 g) were used in three groups, group (1) is a control, group (2) ulcer group, and group(3) (ulcer supplemented group). The duration of the evaluation was 4 weeks. Gastric ulcer was produced by aspirin water suspension (500 mg/kg rat weight). The gene expression of cyclooxygenase-2 (COX-2) and tumor necrosis factor (TNF-α) were determined by RT-PCR. Pomegranate peel powder (10 % w/w) reduced the gastric ulcer area and ulcer index, gastric juice volume, and acidity. Pomegranate powder recovers gastric mucus content and gastric tissue at the histological level. Plasma nitric oxide production was raised while plasma TNF-α level was diminutive by pomegranate peel powder. The gastric mucosal TNF-α and COX-2 gene expression were significantly (p≤ 0.05) down-regulated (2.4 and 12.5 fold-change, respectively) using the pomegranate peel powder. This study introduces pomegranate peel powder (10%) as a protective food supplement against gastric ulcers.

Protective effect of against ethanol-induced gastric ulcer and its mechanism.

: To investigate the protective effect of (FD) against ethanol-induced gastric ulcer and its mechanism. : Human gastric epithelial GES-1 cells were divided into normal control group, model control group, FD 95% alcohol extract group, FD 50% alcohol extract group and FD decoction extract group. Gastric ulcer was induced by treatment with 1% ethanol in GES-1 cells. The cell proliferation was detected with MTT method in each group. Sixty SD rats were randomly divided into normal control group, model control group, ranitidine group and low-dose, medium-dose, high-dose FD 95% alcohol extract groups (150, 300, 600 mg/kg). The corresponding drugs were administrated by gavage for The gastric ulcer model was induced by intragastric administration of anhydrous ethanol. The gastric ulcer area and ulcer inhibition rate of rats were measured in each group; the degree of gastricmucosal damage was observed by scanning electron microscopy; the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β in serum and the content of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), catalase (CAT) in gastric tissues were detected by ELISA method. : 95% alcohol extract of FD had the strongest protective effect on proliferation of GES-1 cells. In animal experiments, compared with the normal control group, a large area of ulcers appeared on the gastric mucosa in the model control group, while the ulcer areas of the FD groups and ranitidine group were significantly smaller than that of the model control group (all <0.05). Compared with the model control group, FD groups and ranitidine group significantly reduced the levels of TNF-α, IL-1β, IL-6 in serum and the MDA content in the gastric tissues, and increased the activity of SOD, CAT and GSH in gastric tissues (all <0.05). : The 95% alcohol extract of FD can reduce the levels of TNF-α, IL-1β and IL-6 in serum and the content of MDA in gastric tissues, and increase the activity of SOD, CAT and GSH in gastric tissues to achieve the protective effect against gastric ulcer.

Activation of AMPK/mTOR-driven autophagy and inhibition of NLRP3 inflammasome by saxagliptin ameliorate ethanol-induced gastric mucosal damage

AimsSaxagliptin, a selective/potent dipeptidyl peptidase-4 inhibitor, has revealed remarkable anti-inflammatory features in murine models of nephrotoxicity, hepatic injury, and neuroinflammation. However, its potential effect on ethanol-induced gastric mucosal injury has not been examined. Hence, the present work investigated the prospect of saxagliptin to attenuate ethanol-evoked gastric injury, with emphasis on the AMPK/mTOR-driven autophagy and NLRP3/ASC/caspase-1 pathway. Materials and methodsIn ethanol-induced gastropathy, the gastric tissues were examined by immunohistochemistry, immunoblotting, histopathology, and ELISA. Key findingsThe results demonstrated that saxagliptin (10 mg/kg; by gavage) suppressed the gastric pathological signs (area of gastric ulcer and ulcer index scores), histopathologic aberrations/damage scores, without provoking hypoglycemia in rats. These protective features were attributed to the enhancement of gastric mucosal autophagy flux, as proven with increased expression of LC3-II and Beclin 1, decreased accumulation of p62 SQSTM1, and activation of the autophagy-linked AMPK/mTOR pathway by increasing the expression of p-AMPK/AMPK and decreasing the expression of the autophagy suppressor p-mTOR/mTOR signal. In tandem, saxagliptin counteracted the ethanol-induced pro-apoptotic events by downregulating Bax, upregulating Bcl2 protein, and lowering the Bax/Bcl2 ratio. Equally important, saxagliptin suppressed the NLRP3 inflammasome in the gastric tissue by lowering the expression of NLRP3, ASC, and nuclear NF-κBp65, decreasing the activity of caspase-1, and diminishing the IL-1β levels. In the same regard, saxagliptin suppressed the mucosal oxidative stress by lowering lipid peroxide levels, increasing GSH and GPx antioxidants, and activating Nrf2/HO-1 pathway. SignificanceSaxagliptin may be a promising intervention against ethanol-evoked gastropathy by activating AMPK/mTOR-driven autophagy and inhibiting NLRP3 inflammasome.

STRESS-PROTECTIVE EFFECTS OF NEW MEDICINAL FORM WITH GLYCINE AND MAGNESIUM CITRATE

Introduction. Stress disorders are common in clinical practice, and their treatment requires selective medication choice. Among the drugs having anxiolytic and sedative effects, glycine and magnesium compounds are being intensively investigated and the options of producing sublingual tablets based on these substances seem to be promising. The aim of this study is to investigate the effects of glycine and magnesium citrate and their combination on glycine and magnesium citrate on somatic parameters (Selye's triad) under the stress conditions and to determine the most effective composition of the compounds.&#x0D; Materials and methods. The experiments were carried out on 76 white rats. The substances were administered sublingually and then the animals were kept in the small cages for 6 hours in order to simulate immobilization stress. At the end of the stress exposure, the rats were euthanized and the relative masses of the thymus and adrenal glands as well as a presence of ulcers and haemorrhages in the stomach were determined. Statistical processing was performed using the Statistica for Windows 8.0 software.&#x0D; Results and discussion. Immobilization stress resulted in a decrease in the relative weight of the thymus in the rats without significant changes in the weight of the adrenal glands and intense ulceration in the stomach. Prophylactic use of the compounds under the study and their combinations prevented the stress-induced involution of the thymus. The most pronounced protective effect was demonstrated by the combination of 100 mg glycine and 250 mg magnesium citrate and glycine itself. At the same time, the relative mass of the adrenal glands did not change significantly. The lowest incidence of ulcerative lesions was observed in the groups of animals who received the combinations of glycine (100 mg) and magnesium citrate (250-350 mg) or glycine (100 mg) separately. This scheme leads to a decrease in the number and area of gastric ulcers as compared to the control group. Magnesium citrate in doses of 250 mg and 350 mg was found not as effective in protecting the gastric mucosa.&#x0D; Conclusion. Acute immobilization stress causes involution of the thymus and gastric ulceration, but does not result in adrenal hypertrophy. According to the findings obtained by the Selye triad study, a combination of 100 mg glycine and 250 mg magnesium citrate and glycine separately in a dose of 100 mg have showed the highest prophylactic effect.