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Color (A), petechiae (B), edema (C), hemorrhage (D) and mucus loss (E) indexes (magnification of 10×) of stomach from rats treated with ethanol and/or omeprazole or Scutia buxifolia extract. Data are means+SD (n=6). Significant difference when compared to water control group (*P<0.01); significant difference when compared to ethanol control group (#P<0.01, ##P<0.001).
Source publication
Gastric ulcers affect many people around the world and their development is a result of the imbalance between aggressive and protective factors in the gastric mucosa. Scutia buxifolia, commonly known as coronilha, has attracted the interest of the scientific community due to its pharmacological properties and its potential therapeutic applications....
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Citations
... 4,17,19 Ethanol stimulation leads to significant ROS production in the gastric mucosa, resulting in increased lipid peroxidation, causing hemorrhagic injury and cellular death. 20 MDA is the endproduct of lipid peroxidation under conditions of high oxidative stress, which promotes partial protein denaturation and enzyme inactivation. Therefore, MDA levels directly indicate the level of lipid peroxidation in vivo and indirectly reflect the severity of cellular injury caused by oxygen free radical attack. ...
BACKGROUND
Dendrobium officinale flos (DOF), a novel food raw material, is used in Chinese folk medicine to nourish the stomach. However, there is still no available study to evaluate the effects of DOF on animal models of acute gastric injury and its mechanism by modern pharmacological research.
RESULTS
Herein, we characterized the major components of an aqueous extract of DOF and assessed its potential ameliorative effects in a rat model of acute gastric mucosal injury. The DOF water extract showed significant protective effects on the gastric mucosa and exhibited excellent antioxidant and anti‐inflammatory activities. Acute gastric injury rat models induced by ethanol (6 mL kg⁻¹) were pretreated with different doses of DOF water extract (50–100 mg kg⁻¹ day⁻¹), and the biological effects of DOF extract in gastric tissues were evaluated. DOF extract alleviated the symptoms of ethanol‐stimulated acute gastric mucosal injury, as evidenced by a significant reduction in gastric injury index and the degree of gastric pathological changes. Additionally, treatment with DOF extract upregulated mucin expression in the gastric mucosa, attenuated oxidative stress, decreased the release of inflammatory mediators (TNF‐α, IL‐6), suppressed the expression of key proinflammatory enzymes (COX‐2 and iNOS), reduced the phosphorylation of p38 MAPK and p65 NF‐κB and increased the level of PGE2 in gastric tissues.
CONCLUSION
DOF exerts protective effects against ethanol‐induced acute gastric mucosal injury, mainly by inhibiting inflammation and oxidative stress. © 2024 Society of Chemical Industry.
... In severe cases, it can lead to the gastric perforation, characterized by a prolonged course and a high recurrence rate (1). Modern research has identified an association between GU and an imbalance of protective and attack factors in the gastric mucosa, suggesting that assessing these levels can help evaluate the pathological process of GU (2). Recently, with the growth of the breeding and pet industries, there has been an increase in the incidence of GU among livestock, poultry, and pets, including bovine gastritis; chicken gastritis; and GUs in cats and dogs. ...
... Differential expression analysis data, GSE76588 for GU, were obtained from the GEO database (NCBI). 2 The species was set to "Rattus norvegicus, " and expression profiles from 6 healthy rats and 14 GU rat samples were retrieved. Chip data analysis was conducted using the limma package in R software, which included batch calibration. ...
Objective
Guanyu Zhixie Granule (GYZXG) is a traditional Chinese medicine compound with definite efficacy in intervening in gastric ulcers (GUs). However, the effect mechanisms on GU are still unclear. This study aimed to explore its mechanism against GU based on amalgamated strategies.
Methods
The comprehensive chemical characterization of the active compounds of GYZXG was conducted using UHPLC-Q/TOF-MS. Based on these results, key targets and action mechanisms were predicted through network pharmacology. GU was then induced in rats using anhydrous ethanol (1 mL/200 g). The intervention effects of GYZXG on GU were evaluated by measuring the inhibition rate of GU, conducting HE staining, and assessing the levels of IL-6, TNF-α, IL-10, IL-4, Pepsin (PP), and epidermal growth factor (EGF). Real-time quantitative PCR (RT–qPCR) was used to verify the mRNA levels of key targets and pathways. Metabolomics, combined with 16S rRNA sequencing, was used to investigate and confirm the action mechanism of GYZXG on GU. The correlation analysis between differential gut microbiota and differential metabolites was conducted using the spearman method.
Results
For the first time, the results showed that nine active ingredients and sixteen targets were confirmed to intervene in GU when using GYZXG. Compared with the model group, GYZXG was found to increase the ulcer inhibition rate in the GYZXG-M group (p < 0.05), reduce the levels of IL-6, TNF-α, PP in gastric tissue, and increase the levels of IL-10, IL-4, and EGF. GYZXG could intervene in GU by regulating serum metabolites such as Glycocholic acid, Epinephrine, Ascorbic acid, and Linoleic acid, and by influencing bile secretion, the HIF-1 signaling pathway, and adipocyte catabolism. Additionally, GYZXG could intervene in GU by altering the gut microbiota diversity and modulating the relative abundance of Bacteroidetes, Bacteroides, Verrucomicrobia, Akkermansia, and Ruminococcus. The differential gut microbiota was strongly associated with serum differential metabolites. KEGG enrichment analysis indicated a significant role of the HIF-1 signaling pathway in GYZXG’s intervention on GU. The changes in metabolites within metabolic pathways and the alterations in RELA, HIF1A, and EGF mRNA levels in RT-qPCR experiments provide further confirmation of this result.
Conclusion
GYZXG can intervene in GU induced by anhydrous ethanol in rats by regulating gut microbiota and metabolic disorders, providing a theoretical basis for its use in GU intervention.
... 4 The causes of gastric ulcer include psychiatric factors, nonsteroidal anti-inflammatory drugs and alcohol. [5][6][7] Gastric mucosal injury is often caused by excessive alcohol intake, and therefore gastric ulcer rat models induced by ethanol are frequently used to evaluate anti-ulcer drugs. Heavy alcohol intake disrupts gastric secretory function, decreasing mucus production, 8 and also generates excessive oxidative factors and inflammatory responses. ...
... Heavy alcohol intake disrupts gastric secretory function, decreasing mucus production, 8 and also generates excessive oxidative factors and inflammatory responses. 5,[9][10][11] Oxidative stress is implicated in gastrointestinal mucosal injury. 12,13 Controlling oxidative stress is essential for the treatment of this pathology. ...
Background
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.
Methods
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.
Results
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 H 2 O 2 ‐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 H 2 O 2 .
Conclusion
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.
... 1 As 10% of the global population is affected by GU, its control and earlier detection are regarded as major obstacles. 2,3 Nearly 15 deaths per 15,000 challenges occur as a result of such events annually worldwide. 1,4,5 An imbalance between gastrointestinal defensive factors and aggressive physical, pharmacological, or psychological variables on the epithelium of the mucous membrane is a common cause of benign lesions such as gastric ulcers. ...
Background
Gastric ulcers pose a significant health risk due to an imbalance between protective and aggressive factors on the mucous membrane. Nonsteroidal anti-inflammatory drug (NSAID)-induced gastric damage affects 25% of users. Quinoxaline compounds, known for their diverse biological properties, have potential applications in cancer therapy and as antimicrobial agents targeting various pathogens.
Objective
Our study aimed to investigate the impact of DMQ on gastroprotective mechanisms in an experimental model of indomethacin-induced gastric ulcer.
Methods
Thirty male Wistar rats were randomly assigned to five groups. Group 1 served as the control, while Group 2 received a single oral dose of IND (30 mg/kg). Groups 3 and 4 received oral DMQ (30 mg/kg and 60 mg/kg, respectively) for three days, with the final dose administered intragastrically one hour before IND administration. Group 5 received esomeprazole (30 mg/kg) orally for three days, with the final dose given one hour before IND administration. Rats were sacrificed four hours after IND induction.
Results
Indomethacin-induced ulcers were associated with epithelial damage and blood streaks on the gastric mucosa. However, DMQ significantly decreased levels of inflammatory biomarkers (TNF-α, IL-6, Cox-2, IFN-γ, and IL-β1) while increasing gastroprotective mediator prostaglandin E2 (PGE2) and mucin levels. Histopathological analysis revealed a significant reduction in ulcer-induced pathological alterations and upregulation of tumor suppressor genes (NF-κB levels) following DMQ treatment. Rats treated with Indo+DMQ showed a significant decrease in ulcer index compared to the Indo group, with mild injuries observed.
Conclusion
DMQ demonstrated promising gastroprotective effects against IND-induced gastric ulcers, as evidenced by alterations in histopathological data and upregulation of gene expression.
... Thus, in the present investigations, the animals received 0.5 mL/100g b.w of liquid (EtOH or water) in the gastric ulcer induction stage + 0.5 mL/100g b.w in the treatment stage. Omeprazol (OMEP) was used as a positive control (BOLIGON et al., 2014) as it is a standard drug used for the clinical treatment of gastric ulcers. ...
... After 7 days of acclimatization, rats were fasted for 12 h to ensure an empty stomach and efficient induction of gastric lesions. Gastric lesions were induced by an oral administration of 75% EtOH (0.5 mL/ 100 g b.w.) (BOLIGON et al., 2014). One hour after EtOH administration, the animals received the treatments (water, FOB, FOB-MP, or OMEP) by gavage. ...
... , which is in accordance with previous reports of this model(BOLIGON et al., 2014;DA SILVA ...
Previous investigations have revealed that a functional fermented orange beverage presented in its composition different phenolic compounds, which through in silico investigation demonstrated to have biological effects of therapeutic importance as antioxidant, gastrorepair, and anti-ulcerative properties. Thus, this study confirmed in vivo, through a model of EtOH-induced gastric ulcers in rats, the beneficial properties indicated by the in silico tests. Gastric ulcer was induced by EtOH (intragastric) and was treated after 1 h with fermented orange beverage with and without Menthapiperita extract (0.5 mL/100 g w.b). Omeprazole was used as positive control. Histopathological evaluation revealed that EtOH administration resulted in the formation of gastric ulcers due to the reduction of the mucus layer, presence of hemorrhage, and infiltration of neutrophils in the stomach tissue of rats, and only treatment with omeprazole was able to reverse these changes. Additionally, EtOH administration altered the gastric juice volume and induced oxidative stress in the gastric tissue observed through the increase in lipid peroxidation (TBARS), reduction in the levels of non-protein thiols (NPSH), and alteration in the superoxide dismutase (SOD) activity. The ingestion of the fermented orange beverage increased NPSH levels and reduced changes in TBARS levels induced by ethanol. These findings suggested that the fermented orange beverage has antioxidant effects, as pointed out by in silico studies, but not gastrorepair and anti-ulcerative effects.
... EtOH/HCl-induced gastric ulcer in rats is a model widely used to evaluate the anti-gastric ulcer effects of test compounds. It has been reported that ethanol induces gastric ulcer formation by decreasing gastric mucous production, mucosal blood flow, and endogenous antioxidants [56,57]. Ethanol increases generation of ROS, the oxidative stress [56][57][58][59], and local inflammatory response by inducing over-secretion of pro-inflammatory mediators and cytokines [59][60][61]. ...
... It has been reported that ethanol induces gastric ulcer formation by decreasing gastric mucous production, mucosal blood flow, and endogenous antioxidants [56,57]. Ethanol increases generation of ROS, the oxidative stress [56][57][58][59], and local inflammatory response by inducing over-secretion of pro-inflammatory mediators and cytokines [59][60][61]. HCl induces gastric mucosal damage via direct irritation and increasing oxidative stress [62]. ...
In Thai traditional medicine, Pikad Tri-phol-sa-mut-than has long been used to alleviate gastrointestinal symptoms, renal disease, inflammation-related disorders, and severe malady. This recipe is composed of dried fruits of Morinda citrifolia L., Coriandrum sativum L., and Aegle marmelos (L.) Corrêa. The aim of this study was to assess the anti-gastric ulcer property of the water extract of Pikad Tri-phol-sa-mut-than (TS), using various animal models with different inducers, including restraint water immersion stress, indomethacin, and ethanol/hydrochloric acid (EtOH/HCl). Its mechanisms of anti-gastric ulcer actions were also elucidated using both in vitro and in vivo experiments. When compared with the control groups, the oral pretreatment of TS at the doses of 150, 300 and 600 mg/kg significantly reduced the gastric ulcer formation in all models. It was also found that TS at the dose of 600 mg/kg could increase gastric wall mucus in rats but could not produce the significant reduction of the gastric volume or total acidity of gastric content. Results from hematoxylin and eosin (H&E) and Periodic acid-Schiff (PAS) staining examinations of gastric tissues confirmed that TS visibly reduced gastric mucosal damage, while immunohistochemistry revealed that TS remarkably suppressed the protein expression of Bcl-2-associated X (BAX), a regulator of apoptosis, compared to those of the control group. The DPPH, ABTS, and FRAP assays showed antioxidant effects of TS. All of these findings demonstrated that TS has gastroprotective effects, which may be related to the increase in the gastric wall mucus secretion, not anti-secretory activity, as well as its antioxidant and antiapoptotic activities.
... "One of the most prevalent gastrointestinal tract disorders, gastric ulcers affect about 5% of the global population and have a mortality rate of one death per 10,000 cases. A number of factors, including an imbalance between aggressive and intrinsic defensive factors, have been linked to its development" [1][2][3]. "Alcohol, NSAIDs, mental stress, and Helicobacter pylori infection are among the aggravating factors. Cytoprotective intrinsic factors include mucosal blood flow, bicarbonate, mucus, cell renewal, growth hormones, NO, and prostaglandins" [4,5]. ...
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.
... Loss of normal mucus color with the presence of signs of necrosis and hemorrhages in the gastric mucosa [28] . These lesions are most likely related to the depletion of mucus and a constrictive effect on veins and arteries in the gastric mucosa, decreasing blood flow and thus producing congestion and inflammation [29] . Furthermore, hydrochloric acid can be self-harming, as it can disrupt gastric epithelial integrity to cause bleeding and/or perforation and likely trigger a local inflammatory response [30] . ...
... IT was also diminished by pre-treatment with CFEE which underscores the gastro-protective capacity of CFEE since less gastric motility leads to a lower percentage of gastric mucosal damage. Phenolic constituents of CFEE might be involved in lowering the gastric motility by impacting α 2 -adrenergic and calcium-mediated action, as was the case for loperamide, an opioid-receptor agonist used to decrease the frequency of diarrhea (Holowacz et al., 2016) and flavonoids such as kaempferol and myricetin (Boligon et al., 2014). ...
... It has been well known that lower ulcerogenic risk of the compounds is combined with a reduced TBARS content in the affected area of the gastrointestinal tract, by products of lipid peroxidation. Therefore, an attempt was made to correlate the decrease in ulcerogenic effect of the compounds with that of lipid peroxidation [26] . The compounds 11 and 12 showed good antioxidant activity compared to other compounds. ...
