Ethanol-induced Gastric Ulcer Research Articles

Protective effects of esomeprazole, curcumin, chitosan, and curcumin-chitosan mixture on ethanol-induced gastric mucosal injuries in female rats

Gastric ulcer is the most common health concern due to alcohol consumption, smoking, and physiological stress. An ethanol-induced gastric ulcer in an animal model resembles the pathophysiology of the human ulcer. The present study attempted to detect the protective effects of esomeprazole, curcumin, chitosan, and a mixture of curcumin and chitosan on ethanol-induced gastric ulcers in female rats. The present study included 60 rats with an average weight between 179.1 and 180.3 g, divided into two control groups and four treated groups (esomeprazole, curcumin, chi¬tosan, and mixture), where each group included 10 rats. All groups were treated for 30 days. In order to induce a gastric ulcer, absolute ethanol (2 mL/rat) was given orally to all groups (except the negative control ones) after a period of fasting of 20 h. All animals were sacrificed 5 h later. The gastric ulceration was studied by comparing the volume and the pH of the gastric juice, the ulcer index as well as the protective index. Our results revealed a significant decrease (P<0.05) in the values of the ulcer index and the volume of gastric juice in the esomeprazole-, curcumin-, chitosan-, and mixture-treated rats as compared to those of the positive control group. The value of the gastric juice pH exhibited a significant increase (P<0.05) in these same groups.

Albizzia chinensis (Osbeck) Merr extract YS ameliorates ethanol-induced acute gastric ulcer injury in rats by regulating NRF2 signaling pathway.

Around the world, there is a high incidence of gastric ulcers. YS, an extract from the Chinese herb Albizzia chinensis (Osbeck) Merr, has potential therapeutic applications for gastrointestinal diseases. Here we elucidated the protective effect and underlying mechanism of action of YS on gastric ulcer in rats injured by ethanol. The ethanol-induced gastric ulcer rat model was used to assess the protective effect of YS. A pathological examination of gastric tissue was performed by H&E staining. GES-1 cells damaged by hydrogen peroxide were used to simulate oxidative damage in gastric mucosal epithelial cells. Endogenous NRF2 was knocked down using small interfering RNA. Immunoprecipitation was used to detect ubiquitination of NRF2. Co-immunoprecipitation was used to detect the NRF2-Keap1 interaction. YS (10 and 30 mg/kg, i.g.) significantly reduced the ulcer index, decreased MDA level, and increased SOD and GSH levels in gastric tissues damaged by ethanol. YS promoted NRF2 translocation from cytoplasm to nucleus and enhanced the NQO1 and HO-1 expression levels in injured rat gastric tissue. In addition, YS regulated NQO1 and HO-1 via NRF2 in H2O2-induced oxidative injured GES-1 cells. Further studies on the underlying mechanism indicated that YS reduced the interaction between NRF2 and Keap1 and decreased ubiquitylation of NRF2, thereby increasing its stability and expression of downstream factors. NRF2 knockdown abolished the effect of YS on MDA and SOD in GES-1 cells treated with H2O2. YS reduced the NRF2-Keap1 interaction, promoting NRF2 translocation into the nucleus, which increasing the transcription and translation of NQO1 and HO-1 and improved the antioxidant capacity of rat stomach.

The Therapeutic Potency of Silver/Chitosan, Silver/Saponin and Chitosan/ Saponin Nanocomposites on Ethanol-induced Gastric Ulcers in Wistar Rats

The Therapeutic Potency of Silver/Chitosan, Silver/Saponin and Chitosan/ Saponin Nanocomposites on Ethanol-induced Gastric Ulcers in Wistar Rats

Retraction Note: The gastro protective effects of Cibotium barometz hair on ethanol-induced gastric ulcer in sprague-dawley rats

Retraction Note: The gastro protective effects of Cibotium barometz hair on ethanol-induced gastric ulcer in sprague-dawley rats

Solanum melongena peels against ethanol-induced gastric ulcer in rats via regulating mucosal enzymes, oxidative stress and inflammatory mediators' pathways

Solanum melongena peels against ethanol-induced gastric ulcer in rats via regulating mucosal enzymes, oxidative stress and inflammatory mediators' pathways

Fish oil ameliorates ethanol-induced gastric injury in rat by modulating gene related to apoptosis

Gastric ulcers are a type of digestive disease that can severely affect a person's quality of life. Our study aimed to investigate the effects of fish oil on ethanol-induced gastric ulcers in rats, with the purpose of providing more comprehensive information on the topic. The study looked at various factors such as gastric ulcer index, and nitric oxide (NO) levels in stomach tissue. To investigate apoptosis, the mRNA levels of Bax, Bcl-2, and Caspase 3 were analyzed. The results showed that fish oil can reduce gastric acidity and the gastric ulcer index in cases of ethanol-induced gastric ulcers. It was found that fish oil can increase NO levels and improve the anti-apoptotic system by increasing the expression of Bcl-2 while decreasing the expression of Bax and Caspase 3. In general, the study demonstrates that fish oil can protect the stomach from ethanol-induced damage by reducing the apoptosis pathway via nitric oxide.

Aloe vera gel confers therapeutic effect by reducing pyroptosis in ethanol-induced gastric ulcer rat model: Role of NLRP3/GSDMD signaling pathway

BackgroundGastric ulcer (GU) is a common gastrointestinal tract illness. Aloe vera has anti-inflammatory, antioxidant, and healing characteristics. This research sought to explore the therapeutic impact of Aloe vera gel on ethanol-provoked GU in rats and to elucidate the underlying mechanisms involved.MethodsAn ethanol-induced GU rat model was constructed using forty male Wistar rats distributed at random into four groups: control, ulcer, pantoprazole, and Aloe vera. Gross evaluation of the stomach, ulcer index (UI), inhibition index, and gastric pH estimation were analyzed. Gastric malondialdehyde (MDA) and reduced glutathione (GSH) were determined using the spectrophotometric method, and serum gastrin level was measured by an enzyme-linked immunosorbent assay. Gastric nucleotide-binding domain, leucine-rich repeat, and pyrin domain PYD containing protein 3 (NLRP3) and gasdermin D (GSDMD) mRNA expression levels were estimated by quantitative real-time PCR. Finally, the histopathological examination of the glandular part of stomach tissue was done.ResultsThe ulcer group revealed a significant increase in MDA, gastrin, NLRP3, and GSDMD and a decrease in gastric pH and GSH compared to the control group. Gross investigations of the ulcer group revealed a hemorrhagic lesion in the stomach and an increase in UI. Also, histopathological results for this group showed severe epithelial loss, haemorrhage, inflammatory cell infiltration, and blood vessel congestion. However, Aloe vera treatment improved the gross, biochemical, molecular, and histopathological alterations induced by ethanol when compared to the ulcer group.ConclusionsAloe vera exerted antiulcer activities through modulation of oxidant/antioxidant status, anti-secretory properties, and mitigation of pyroptosis.

Enhanced upregulation of SIRT1 via pioglitazone and ligustrazine confers protection against ethanol-induced gastric ulcer in rats.

Gastric ulcer is a disturbing disease that impacts many people worldwide. Pioglitazone (Piog), a thiazolidinedione, and ligustrazine (Ligu), a natural component of Ligusticum chuanxiong possess gastroprotective properties. However, the underlying mechanism is not well elucidated. The present study aimed to investigate the gastroprotective effects of Piog (15 mg/kg, p.o.), Ligu (15 mg/kg, p.o.), and their combination against ethanol-induced gastric ulcer in rats. Omeprazole (10 mg/kg) was used as a standard. Pre-treatment for 7 days with Piog, Ligu, and (Piog+Ligu) effectively alleviated ethanol-predisposed oxidative stress and inflammation through restoring HO-1, GSH, and SOD tissue levels and decreasing elevated MDA, TNF-α, ICAM, I-NOS, and IL-1β contents. Moreover, Piog, Ligu, and (Piog+Ligu) markedly inhibited the ethanol-induced increase of gastric NF-KB and BAX. In contrast, this pre-treatment regimen significantly accelerated protein expression of SIRT1, Nrf2, and Bcl-2, along with autophagic proteins, ATG5 and Beclin. Interestingly, macroscopic, histopathological examination and mucin content were in harmony with previous results, where pre-treatment with Piog, Ligu, and (Piog+Ligu) showed a declined mucosal injury as evidenced by the remarkable decrease of the ulcer area percentage by 62.3%, 38.7%, and 91.2%, respectively, compared to the ethanol-ulcerated group. In conclusion, Piog and Ligu exhibited remarkable gastroprotective properties. Our study was the first to show that Piog, Ligu, and (Piog+Ligu) ameliorated oxidative stress, inflammation, and apoptosis and accelerated the autophagic process via the upregulation of the upstream SIRT1 protein. It is worth mentioning that future studies are needed to pave the way for the clinical use of Piog and Ligu as gastro-protective agents.

In vitro true root cultures of Lotus hebranicus Hochst. ex brand: profiling of secondary metabolites and plausible in vivo gastroprotective effect

In vitro, the Lotus hebranicus produces true root cultures under entirely growth regulator-free culture conditions. These roots are completely independent of the shoots and gives abundant amounts of biomass of true root culture as raw materials in a short time. Lately, gastric ulcer have gained an increasing interest as it affects millions around the world. So, this study aimed to screen and evaluate the chemical constituents of the L. hebranicus extract (plant and true root culture), in addition to studying the biological effect of these extracts on mice with ethanol-induced gastric ulcer and the possible role of mediating oxidative stress, inflammation and TGFβ/Smad3 as underlying mechanisms. Fifty-four Albino mice were assigned into nine groups (n = 6). Lotus was orally administered for seven successive days, followed by a single dose of oral ethanol for ulcer induction. Using histological assessment and immunohistochemical studies as well as colorimetric analysis, ELISA and qRT-PCR, the results revealed that ethanol-induced ulcers exhibited a substantial increase (p < 0.05) in malondialdehyde and interleukin 18 with a remarkable lessening in the gastro-protective mediators; superoxide dismutase, prostaglandin E2 and glutathione, parallel with an increase in TGFβ/Smad3 expressions relative to control. Pre-treatment with L. hebranicus showed a comparable result to those with omeprazole and showed a significant inhibitory effect on inflammatory mediators and significant elevation of the gastro-protective mediators relative to the positive control. In conclusion, L. hebranicus extract (plant/true root culture) has the potential to protect the gastric tissues against ethanol by inhibiting oxidative stress and inflammation and enhancing TGFβ/Smad3 mediators along with gastric protective mediators.

Ipomoea carnea mitigates ethanol-induced ulcers in irradiated rats via Nrf2/HO−1 pathway: an in vivo and in silico study

The aim of this study was to investigate the potential of Ipomoea carnea flower methanolic extract (ICME) as a natural gastroprotective therapy against ethanol-induced gastric ulcers, particularly in individuals exposed to ionizing radiation (IR). The study focused on the Nrf2/HO−1 signaling pathway, which plays a crucial role in protecting the gastrointestinal mucosa from oxidative stress and inflammation. Male Wistar rats were divided into nine groups, the control group received distilled water orally for one week, while other groups were treated with ethanol to induce stomach ulcers, IR exposure, omeprazole, and different doses of ICME in combination with ethanol and/or IR. The study conducted comprehensive analyses, including LC-HRESI-MS/MS, to characterize the phenolic contents of ICME. Additionally, the Nrf2/HO−1 pathway, oxidative stress parameters, gastric pH, and histopathological changes were examined. The results showed that rats treated with IR and/or ethanol exhibited histopathological alterations, increased lipid peroxidation, decreased antioxidant enzyme activity, and reduced expression levels of Nrf2 and HO−1. However, pretreatment with ICME significantly improved these parameters. Phytochemical analysis identified 39 compounds in ICME, with flavonoids, hydroxybenzoic acids, and fatty acids as the predominant compounds. Virtual screening and molecular dynamics simulations suggested that ICME may protect against gastric ulceration by inhibiting oxidative stress and inflammatory mediators. In conclusion, this study demonstrates the potential of ICME as a natural gastroprotective therapy for preventing gastric ulcers. These findings contribute to the development of novel interventions for gastrointestinal disorders using natural plant extracts particularly in individuals with a history of radiation exposure.

The active components and potential mechanisms of Wuji Wan in the treatment of ethanol-induced gastric ulcer: An integrated metabolomics, network pharmacology and experimental validation

Ethnopharmacological relevanceWuji Wan (WJW) is a traditional Chinese medicine formula that can be found in the "Prescriptions of Taiping Benevolent Dispensary" that has been employed in treating gastric discomfort, burning epigastric pain, and gastric reflux for hundreds of years and has shown promise for treating gastric ulcers (GUs). However, the active components and mechanism of action against GUs remain unclear. Aim of the studyThe aim of this study was to explore the active components of WJW and elucidate the underlying mechanism involved in treating GUs. Materials and methodsInitially, cell viability was measured by a cell counting kit 8 (CCK-8) assay to evaluate the efficacy of WJW-containing serum in vitro. The gastric ulcer index, ulcer inhibition rate, hematoxylin and staining (H&E), and periodic acid-Schiff (PAS) staining were used to evaluate the therapeutic effect of WJW in vivo. Subsequently, the levels of inflammatory factors and oxidative stress factors were determined using an enzyme-linked immunosorbent assays (ELISA) on in vitro and in vivo samples. Additionally, UPLC-Q Exactive Plus Orbitrap HRMS was used to analyze the components that were absorbed into the blood of WJW and its metabolites. Network pharmacology and metabolomics were subsequently used to identify the targets and pathways. Real-time quantitative PCR (RT‒qPCR) and Western blotting were used to verify the mRNA and protein levels of the key targets and pathways. Finally, the active components were identified by molecular docking to verify the binding stability of the components and key targets. ResultsWJW-containing serum ameliorated ethanol-induced damage in GES-1 cells and promoted cell healing. WJW-containing serum reduced IL-6, TNF-α, MDA, and LDH levels while increasing IL-10, SOD, and T-AOC levels in the cells. Moreover, WJW treatment resulted in decreased IL-6, TNF-α, and MDA levels and increased IL-10, SOD, PGE2, and NO levels in GUs rats. In addition, eight components of WJW were absorbed into the blood. The network pharmacology results revealed 192 common targets for blood entry components and GUs, and KEGG analysis revealed that apoptosis signaling pathways were the main pathways involved in WJW activity against GUs. Metabolomic screening was used to identify 13 differential metabolites. There were 23 common targets for blood entry components, GUs, and differential metabolites, with the key targets TNF (TNF-α), AKT1, PTGS2 (COX2) and MAPK1. WJW significantly inhibited the expression of Bax, Caspase-9, Caspase-3, cleaved Caspase-9, cleaved Caspase-3, TNF-α, COX2, and p-p44/42 MAPK while promoting the expression of Bcl-2 and p-AKT1. Molecular docking revealed that the active components of WJW for the treatment of GUs are berberine, palmatine, coptisine, evodiamine, rutaecarpine, evocarpine, and paeoniflorin. ConclusionsWJW treatment reduces inflammation and oxidative stress injury and inhibits apoptosis signaling pathways. The main active components are berberine, palmatine, coptisine, evodiamine, rutaecarpine, evocarpine, and paeoniflorin. In this paper, we provide a new strategy for exploring the active components of traditional Chinese medicine formulas for the treatment of diseases based on target mechanisms.

Protective effects of an alcoholic extract of Kaempferia galanga L. rhizome on ethanol-induced gastric ulcer in mice

Ethnopharmacological relevanceThe rhizome of Kaempferia galanga L., a medicinal and edible Plant, was widely distributed in many Asian and African counties. It has been traditionally used to treat gastroenteritis, hypertension, rheumatism and asthma. However, there is a lack of modern pharmacology studies regarding its anti-gastric ulcer activity. Aim of the studyThe objective of this study is to investigate the protective effects of an extract from K. galanga L. rhizome (Kge) and its active components kaempferol and luteolin on ethanol-induced gastric ulcer. Materials and methodsThe kge was prepared by ultrasonic-assisted extraction, and the contents of kaempferol and luteolin were determined by HPLC. The mice were randomly divided into seven groups: blank control (0.5 % CMC-Na; 0.1 mL/10 g), untreatment (0.5 % CMC-Na; 0.1 mL/10 g), Kge (100, 200 and 400 mg/kg), kaempferol (100 mg/kg) and luteolin (100 mg/kg) groups. The mice were treated intragastrically once daily for 7 days. At 1 h post the last administration, the mice in all groups except the blank control group were intragastrically administrated with anhydrous alcohol (0.1 mL/10 g) once to induce gastric ulcer. Then, fasting was continued for 1 h, followed by sample collection for evaluation by enzyme-linked immunosorbent assay and real-time reverse transcription polymerase chain reaction assay. ResultsThe contents of kaempferol and luteolin in Kge were determined as 3713 μg/g and 2510 μg/g, respectively. Alcohol induced severely damages with edema, inflammatory cell infiltration and bleeding, and the ulcer index was 17.63 %. After pre-treatment with Kge (100, 200 and 400 mg/kg), kaempferol and luteolin, the pathological lesions were obviously alleviated and ulcer indices were reduced to 13.42 %, 11.65 %, 6.54 %, 3.58 % and 3.85 %, respectively. In untreated group, the contents of Ca2+, myeloperoxidase, malondialdehyde, NO, cyclic adenosine monophosphate and histamine were significantly increased, while the contents of hexosamine, superoxide dismutase, glutathione peroxidase, and prostaglandin E2 were significantly decreased; the transcriptional levels of IL-1α, IL-1β, IL-6, calcitonin gene related peptide, substance P, M3 muscarinic acetylcholine receptor, histamine H2 receptor, cholecystokinin 2 receptor and H+/K+ ATPase were significantly increased when compared with the blank control group. After pre-treatment, all of these changes were alleviated, even returned to normal levels. Kge exhibited anti-gastric ulcer activity and the high dose of Kge (400 mg/kg) exhibited comparable activity to that of kaempferol and luteolin. ConclusionThe study showed that K. galanga L., kaempferol, and luteolin have protective effects against ethanol-induced gastric ulcers. This is achieved by regulating the mucosal barrier, oxidative stress, and gastric regulatory mediators, as well as inhibiting the TRPV1 signaling pathway and gastric acid secretion, ultimately reducing the gastric ulcer index.

Effects of fish oil on ethanol-induced gastric ulcer in rats: inflammatory responses and oxidative stress

Background: The prevalence of peptic ulcers is increasing due to lifestyle changes and harmful diets. Objective: The aim of this study was to investigate the effect of fish oil (FO) on gastric ulcers induced by ethanol in rats. Methods: The pharmacological efficacy of FO with doses of 5 and 10 mg/kg investigated using the gastric ulcer index, the acidity of gastric secretions, pro-inflammatory cytokine assessment, and oxidative stress examination. Results: Ethanol-induced gastric ulcer improves with FO 5 or 10 mg/kg pretreatment (P&lt;0.05). FO did have acid-neutralizing activity. FO also increased the levels of glutathione and catalase and decreased the malondialdehyde levels (P&lt;0.05). Moreover, FO reduced the levels of tumour necrosis factor alpha (TNF-α) interleukin-6 (IL-6), through downregulation of nuclear factor kappa B (NF-κB) (P&lt;0.05). Pretreatment with FO attenuates ethanol-induced gastric ulceration. Conclusion: The observed effects may be due to the role of FO in regulating gastric secretions, changes in the expression of NF-κB, and changes in the levels of oxidative stress factors.

Curcumin regulates inflammation and apoptosis through PARP-1 and NF-κB in ethanol-induced gastric ulcer model

Curcumin regulates inflammation and apoptosis through PARP-1 and NF-κB in ethanol-induced gastric ulcer model

Licorice flavonoid ameliorates ethanol-induced gastric ulcer in rats by suppressing apoptosis via PI3K/AKT signaling pathway

Ethnopharmacological relevanceLicorice is the dry roots and rhizomes of Glycyrrhiza uralensis Fisch., Glycyrrhiza glabra L. and Glycyrrhiza inflata Bat., which was first recorded in Shengnong's herbal classic. Licorice flavonoid (LF) is the main compound isolated from licorice with an indispensable action in treating gastric ulcer (GU). However, the underlying mechanisms need to be further explored. Aim of the studyThis study aimed to investigate and further elucidate the mechanisms of LF against ethanol-induced GU using an integrated approach. Materials and methodsThe anti-GU effects of LF were evaluated in an ethanol-induced gastric injury rat model. Then, the metabolomics approach was applied to explore the specific metabolites and metabolic pathways. Next, the network pharmacology combined with metabolomics strategy was employed to predict the targets and pathways of LF for GU. Finally, these predictions were validated by molecular docking, RT-qPCR, and western blotting. ResultsLF had a positive impact on gastric injury and regulated the expression of GU-related factors. Upon serum metabolomics analysis, 25 metabolic biomarkers of LF in GU treatment were identified, which were primarily involved in amino acid metabolism, carbohydrate metabolism, and other related processes. Subsequently, a “components-targets-metabolites” network was constructed, revealing six key targets (HSP90AA1, AKT1, MAPK1, EGFR, ESR1, PIK3CA) that may be associated with GU treatment. More importantly, KEGG analysis highlighted the importance of the PI3K/AKT pathway including key targets, as a critical route through which LF exerted its anti-GU effects. Molecular docking analyses confirmed that the core components of LF exhibited a strong affinity for key targets. Furthermore, RT-qPCR and western blotting results indicated that LF could reverse the expression of these targets, activate the PI3K/AKT pathway, and ultimately reduce apoptosis. ConclusionLF exerted a gastroprotective effect against gastric ulcer induced by ethanol, and the therapeutic mechanism may involve improving metabolism and suppressing apoptosis through the PI3K-AKT pathway.

Anti H. pylori, anti-secretory and gastroprotective effects of Thymus vulgaris on ethanol-induced gastric ulcer in Sprague Dawley rats.

The objectives of the present study were to evaluate the acute toxicity, gastroprotective, therapeutic, anti-inflammatory and anti H. pylori activities of T. vulgaris total plant extract against ethanol-induced gastric ulcers in Sprague Dawley rats. Animals were divided into five groups i.e G-1 (Normal Control), Group 2 (ulcer control) were administered orally with 0.5% Carboxymethylcellulose (CMC), Group 3 (omeprazole treated) was administered orally with 20 mg/kg of omeprazole and Groups 4 and 5 (Low dose and High dose of the extract) were administered orally with 250, and 500 mg/ kg of Thymus vulgaris extract, respectively. After 1 hour, the normal group was orally administered with 0.5% CMC (5 ml/kg), whereas absolute alcohol (5ml/ kg) was orally administered to the ulcer control group, omeprazole group, and experimental groups. Stomachs were examined macroscopically and microscopically. Grossly, rats pre-treated with T. vulgaris demonstrated significantly decreased ulcer area and an increase in mucus secretion and pH of gastric content compared with the ulcer control group. Microscopy of gastric mucosa in the ulcer control group showed severe damage to gastric mucosa with edema and leukocytes infiltration of the submucosal layer. However, rats pretreated with omeprazole or Thyme vulgaris exhibited a mild to moderate disruption of the surface epithelium and lower level of edema and leukocyte infiltration of the submucosal layer. The T. vulgaris extract caused up-regulation of Hsp70 protein, down-regulation of Bax protein, and intense periodic acid Schiff uptake of the glandular portion of the stomach. Gastric mucosal homogenate of rats pre-treated with T. vulgaris exhibited significantly increased superoxide dismutase (SOD) and catalase (CAT) activities while malondialdehyde (MDA) level was significantly decreased. Based on the results showed in this study, Thymus vulgaris extract can be proposed as the safe medicinal plants for use and it has considerable gastroprotective potential via stomach epithelium protection against gastric ulcers and stomach lesions.

Gastroprotective Chitosan Nanoparticles Loaded with Oleuropein: An In Vivo Proof of Concept.

Oleuropein is the main constituent of olive leaf extract, and it has shown antioxidant and gastroprotective properties against gastric ulcers. Chitosan nanoparticles are known for their mucoadhesive abilities, and consequently, they can increase the retention time of drugs in the gastrointestinal tract. Therefore, loading oleuropein onto chitosan nanoparticles is expected to enhance its biological efficiency. Oleuropein-loaded chitosan nanoparticles were prepared and characterized for particle size, surface charge, in vitro release, and anti-inflammatory activity. Their in vivo efficacy was assessed by measuring specific inflammatory and protective biomarkers, along with histopathological examination. The optimum oleuropein chitosan nanoparticles were cationic, had a size of 174.3 ± 2.4 nm and an entrapment efficiency of 92.81%, and released 70% of oleuropein within 8 h. They recorded a lower IC50 in comparison to oleuropein solutions for membrane stabilization of RBCs (22.6 vs. 25.6 µg/mL) and lipoxygenase inhibition (7.17 vs. 15.6 µg/mL). In an ethanol-induced gastric ulcer in vivo model, they decreased IL-1β, TNF-α, and TBARS levels by 2.1, 1.7, and 1.3 fold, respectively, in comparison to increments caused by exposure to ethanol. Moreover, they increased prostaglandin E2 and catalase enzyme levels by 2.4 and 3.8 fold, respectively. Immunohistochemical examination showed that oleuropein chitosan nanoparticles markedly lowered the expression of IL-6 and caspase-3 in gastric tissues in comparison to oleuropein solution. Overall, oleuropein chitosan nanoparticles showed superior gastroprotective effects to oleuropein solution since comparable effects were demonstrated at a 12-fold lower drug dose, delineating that chitosan nanoparticles indeed enhanced the potency of oleuropein as a gastroprotective agent.

Therapeutic Effects of Esomeprazole, Curcumin, Chitosan, and Curcumin-Chitosan Mixture on Ethanol-Induced Gastric Ulcer in Female Rats

Introduction: Gastric ulcer (GU) is a prevalent health issue linked to alcohol consumption, smoking, and physiological stress. This study aims to assess the therapeutic effects of esomeprazole (40 mg), curcumin (40 mg/kg), chitosan (150 mg/kg), and a mixture of curcumin (40 mg/kg) and chitosan (150 mg/kg) on ethanol-induced gastric ulcers in female rats. Method: The study involved 30 female rats with an average weight ranging from 179.1 to 180.3 gm. Rats were divided into two control groups and four treated groups (esomeprazole, curcumin, chitosan, and mixture), each containing 5 rats. Gastric ulcers were induced by orally administering 2 ml of absolute ethanol to All groups, except the negative control, after a 19-hour fasting period. Therapeutic effects were evaluated by assessing gastric juice volume and pH, ulcer index, curative index, and through morphological and histological examination of the stomach. Results: The study revealed a significant decrease (p≤0.05) in body weight percentage change in the curcumin-treated group compared to the positive control. Esomeprazole, chitosan, and the mixture showed mixture showed no significant change (p&gt;0.05). Additionally, esomeprazole, curcumin, chitosan, and the mixture demonstrated a significant decrease (p≤0.05) in ulcer index and gastric juice volume, with a significant increase (p≤0.05) in pH compared to the positive control. Conclusion: In conclusion, esomeprazole, chitosan, and the mixture demonstrated notable protective effects and therapeutic effects by reducing ulcer index and gastric juice volume in ethanol-induced gastric ulcers in female rats.

Gastroprotective effect of rhodanine and 2,4-thiazolidinediones scaffolds in rat stomachs by contribution of anti-apoptotic (BCL-2) and tumor suppressor (P53) proteins

In recent times, the methods used to evaluate gastric ulcer healing worldwide have been based on visual examinations and estimating ulcer dimensions in experimental animals. In this study, the protective effect of rhodanine and 2,4-thiazolidinediones scaffolds compared to esomeprazole was investigated in an ethanol model of stomach ulcers in rats. Pretreatment with experimental treatments or esomeprazole prevented the development of ethanol-induced gastric ulcers. The severity of the lesions and injuries was significantly lower than that of vehicle (10% Tween 80) treated rats. Significant and excellent results were obtained with the compound 6 group, with inhibition percentage and ulcer area values of 97.8% and 12.8 ± 1.1 mm2, respectively. Synthesized compounds 2, 7 and 8 exhibited inhibition percentages and ulcer areas of 94.3% and 31.2 ± 1.1 mm2, 91. 3% and 48.1 ± 0. 8 mm2, 89. 5% and 57. 6 ± 1. 2 mm2, and 89. 1% and 60.3 ± 0. 8 mm2, respectively. These biological outcomes are consistent with the docking studies in which Compounds 7 and 8 showed remarkable binding site affinities toward human H+/K+-ATPase α protein (ID: P20648), rat H+/K+-ATPase α protein (ID: P09626), and Na+/K+-ATPase crystal structure (PDB ID:2ZXE) with binding site energies of − 10.7, − 9.0, and − 10.4 (kcal/mol) and − 8.7, − 8.5, and − 8.0 (kcal/mol), respectively. These results indicate that these test samples were as effective as esomeprazole. Likewise, immunohistochemical staining of antiapoptotic (BCL2) and tumor suppressor (P53) proteins showed strong positive marks in the10% Tween 80- treated group, opposing the mild staining results for the esomeprazole-treated group. Similarly, the staining intensity of the group treated with Compounds 2–8 was variable for both proteins.

Prevención de úlceras estomacales inducidas por etanol en ratas utilizando extracto de hoja de Senecio perralderianus

Senecio perralderianus belongs to the family of Asteraceae and is only found in Algeria. Some species of this family are used to heal gastrointestinal issues in conventional medicine for their antioxidant and anti-inflammatory properties. This research was performed in order to determine if methanolic extract from the leaves of S. perralderianus had any protective effects on gastroenteritis brought on by alcohol consumption. Wistar rats were fed with 100% ethanol orally to induce gastric ulcer, and pre-treated with 50, 100, and 200 mg·kg-1 of the extract in addition to 5 mg·kg-1 of Ranitidine as a positive reference drug. The extract had shown a positive effect to protect ethanol-induced gastric ulcers with a protection percentage of 71 to 88%. In addition, pretreatment of rats significantly increased levels of GSH, CAT, and SOD in vivo as non-enzymatic and enzymatic antioxidants, and also reduced the level of lipid peroxidation. Histopathological sections, which showed the action of the therapeutic extract, substantially confirmed these findings on the reduction of the inflammation zone and the reduction of immune cell filtration caused by ethanol toxicity with increased extract dosages compared to Ranitidine. The antiulcer activity is due to inhibition of oxidative stress and gastritis. It is associated with a total polyphenol, flavonoids, chlorophyll (a, b), and carotenoids substantial amounts.