Gastric Tissue Damage Research Articles (Page 1)

Health-promoting effects of Clostridium butyricum GKB7 on the gastrointestinal tract in murine models.

Long-term excessive alcohol intake can directly injure the gastroduodenal mucosa, causing gastric erosions, gastric ulcers, and gastrorrhagia. Fritillaria ussuriensis Maxim is a famous traditional Chinese medicine and health food produced in China. Sipeimine is an alkaloidal component of Fritillaria ussuriensis Maxim. This research aimed to investigate the protective effects of sipeimine on ethanol-induced gastric ulcers in mice. The results displayed that sipeimine could alleviate gastric tissue damage and decrease the levels of SOD, MDA, IL-6, IFN-γ, TNF-α, and IL-1β. Sipeimine treatment also adjusted macrophage polarization and the balance of Th17/Treg cell by reducing the expression of Jak1/2, p-Jak1/2, Stat1/3, and p-Stat1/3. Moreover, sipeimine could increase the abundance of Lactobacillus_johnsonii and decrease the abundance of Bacteroides_vulgatus in the gut microbiota. Meanwhile, sipeimine treatment significantly decreased the abundance of Rodentibacter_heylii and Streptococcus_cuniculi in the gastric microbiota. In conclusion, sipeimine can improve gastric ulcers by suppressing the Jak-Stat pathway, reversing gut-gastro microbiota dysbiosis, inhibiting macrophage M1 polarization, maintaining the balance of Th17/Treg cell, and lessening sustained inflammatory injury.

Wenweishu (WWS), a traditional gastritis formula, was studied to elucidate its mechanisms in preventing water immersion restraint stress-induced gastric ulcers (GU) in rats. The degree of gastric tissue damage was assessed in experimental rats based on the gastric mucosal ulcer index and pathological observation. The antioxidant properties of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) were detected in gastric tissues, along with expression levels of inflammatory factors, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. The core components, primary targets, and putative mechanisms of WWS were predicted using network pharmacology and molecular docking and validated via immunohistochemistry and immunoblotting analyses. WWS reduced the ulcer index, increased SOD and GSH-px, and decreased IL-1β, IL-6, TNF-α, and MDA levels. A total of 126 WWS components were identified and associated with 4920 GU-associated targets via network pharmacological analysis. Data from Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed associations of the core targets with multiple pathways, in particular, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling. Molecular docking analysis confirmed significant docking activity of the main bioactive components with the core targets tumor protein (TP53) and protein kinase Bα (AKT1). Immunohistochemistry and Western blot analyses showed that WWS markedly suppressed phosphorylation levels of Akt and PI3K proteins in gastric tissues. WWS exerts a protective effect on the gastric mucosa by inhibiting the PI3K/Akt pathway, attenuating inflammatory factors and oxidative damage. The collective findings provide a scientific basis for the application of WWS in the management of GU.

Potential mechanisms by which Jiawei Lianpu Yin inhibits Helicobacter pylori colonization and alleviates gastric mucosal inflammation and damage: Integrated transcriptomics, network pharmacology, and experimental validation.

Background: This study investigated the antioxidant, hepatoprotective, and sedative modulatory effects of Nigella sativa alcoholic extract (NSAE) in CCl4-induced hepatotoxicity in rats. Methods: Male Wistar rats were divided into six groups (n=6): normal control, CCl4 control, silymarin (50 mg/kg), and NSAE (100, 200, and 400 mg/kg). Hepatoprotective effects were evaluated through biochemical parameters, oxidative stress markers, and histopathological examination. Results: NSAE treatment (400 mg/kg) significantly restored liver function markers, including SGOT (20.95 ± 0.52 IU/L, p = 0.033) and SGPT (28.61 ± 0.67 IU/L, p < 0.001), compared to CCl4 control. Total protein and albumin levels were normalized to 5.68 ± 0.54 mg/dL and 3.84 ± 0.48 mg/dL, respectively. Antioxidant parameters showed marked improvement with NSAE (400 mg/kg), increasing GSH (0.26 ± 0.029 µmol/mg) and CAT (30.19 ± 2.69 µg/mL) while reducing MDA (0.048 ± 0.008 µg/mL). Histopathological examination revealed significant protection against CCl4-induced hepatic and gastric tissue damage, particularly at the 400 mg/kg. Conclusion: NSAE exhibited marked hepatoprotective activity comparable to silymarin, predominantly through antioxidant mechanisms and the maintenance of hepatic tissue integrity, indicating its potential as a natural therapeutic agent for managing liver diseases. Because of its hepatoprotective and antioxidant properties, NSAE may be explored in clinical settings as a natural supplement to traditional liver disease therapies or as a prophylactic for people at risk of liver disorders.

Vitexin alleviates MNNG-induced chronic atrophic gastritis via inhibiting NLRP3 inflammasome.

Sesquiterpene-enriched extract of Chinese agarwood (Aquilaria sinensis) alleviates bile reflux gastritis through suppression of gastric mucosal cell apoptosis via the Wnt/β-catenin signaling pathway

Berberine (BBR), a widely recognized traditional Chinese medicine, has attracted considerable attention for its promising anti‐inflammatory effects. The activation of nuclear factor erythroid 2‐related factor 2 (Nrf2) effectively safeguards against organ damage stemming from sepsis‐induced oxidative stress and inflammatory responses. This study examined the potential of BBR in alleviating sepsis‐induced acute gastric injury, with a particular focus on elucidating whether its mechanism of action involves the activation of the Nrf2 signaling pathway. Following intraperitoneal injection of BBR, mice were subjected to the cecal ligation and puncture (CLP) method to induce sepsis. In vitro experiments involved pre‐treating the normal gastric epithelial cells (GES‐1) with BBR, followed by treatment with lipopolysaccharide (LPS). Functional assays were then performed to assess cell proliferation and apoptosis. To validate the role of Nrf2 in pyroptosis and inflammation, siRNA targeting Nrf2 (si‐Nrf2) was transfected into LPS‐treated GES‐1 cells. Additionally, mice were administered the Nrf2 inhibitor ML385 to confirm the protective effects of BBR in vivo. BBR displayed a dose‐dependent effect in mitigating gastric tissue damage, suppressing the release of inflammatory cytokines, and reducing the expression of NLRP3, ASC, and GSDMD‐N. In vitro, BBR fostered GES‐1 cell proliferation, hindered apoptosis, and suppressed the levels of TNF‐α, IL‐18, IL‐1β, NLRP3, ASC, and GSDMD‐N. Further analysis revealed that knocking down Nrf2 reversed BBR's inhibitory effect on pyroptosis in LPS‐treated GES‐1 cells. Through binding to Keap1, BBR efficiently prevented the ubiquitination and degradation of Nrf2, ultimately promoting its nuclear translocation. In vivo experiments confirmed that ML385 reversed the protective effect of BBR on pyroptosis and inflammation. Our research reveals that BBR interacts with Keap1 to activate the Keap1/Nrf2 signaling pathway in gastric epithelial cells, thereby suppressing pyroptosis and inflammation in sepsis‐induced acute gastric injury.

Effect of antiemetics on zolbetuximab-induced gastric injury and emesis in ferrets

Gastric ulcers are a common gastrointestinal disorder associated with significant morbidity and mortality. It can also increase the risk of gastric cancer. This study aimed to investigate the effect of benfotiamine on experimentally-induced gastric ulcers in male rats. In this study, 30 Wistar male rats were divided randomly into six groups: control (normal), indomethacin, omeprazole, and treatment groups, including 50, 100, and 200mg/kg of benfotiamine. Gastric ulcer was induced by indomethacin gavage. Omeprazole and different therapeutic doses of benfotiamine were administered for three days. Twenty-four hours after the last treatment, the rats were euthanized, and samples were collected.The results demonstrated that 100 and 200mg/kg of benfotiamine treatment significantly improved indomethacin-induced gastric tissue damage. Moreover, benfotiamine at 100 and 200mg/kg effectively attenuated the levels of pro-inflammatory cytokines IL-6 and TNF-α and oxidative stress markers MDA and ROS while increasing the antioxidant GSH. These findings suggest that benfotiamine's gastroprotective effects are mediated through its antioxidant and anti-inflammatory properties, which help mitigate the tissue damage and inflammatory response associated with indomethacin-induced gastric ulcers.However, further research is needed to elucidate the precise molecular mechanisms underlying these beneficial effects and to evaluate the potential therapeutic application of benfotiamine in clinical settings.

Background: Gastric ulcers (GUs) are prevalent digestive disorders worldwide. Wuzhuyu Decoction (WZYT) is a traditional Chinese medicine that has been employed for centuries to alleviate digestive ailments like indigestion and vomiting. This study aims to explore the potential effects and underlying mechanisms of WZYT on alcohol induced gastric ulcer treatment. Methods: We employed macroscopic assessment to evaluate the gastric ulcer index (UI), while the enzyme-linked immunosorbent assay (ELISA) was utilized for detecting biochemical indicators. Pathological tissue analysis involved hematoxylin-eosin (H&E) staining and Periodic Acid-Schiff (PAS) staining to assess gastric tissue damage. Additionally, the integration of network analysis and metabolomics facilitated the prediction of potential targets. Validation was conducted using Western blotting. Results: The research revealed that WZYT treatment significantly reduced the gastric ulcer index (UI) and regulation of alcohol-induced biochemical indicators levels. Additionally, improvements were observed in pathological tissue. Network analysis results indicated that 62 compounds contained in WZYT modulate alcohol-induced gastric ulcers by regulating 183 genes. The serum metabolomics indicated significant changes in the content of 19 metabolites after WZYT treatment. Two pivotal targets, heme oxygenase 1 (HMOX1) and albumin (ALB), are believed to assume a significant role in the treatment of gastric ulcers by the construction of "compounds-target-metabolite" networks. Western blot analysis confirmed that WZYT has the capacity to elevate the expression of HMOX1 and ALB targets. Conclusion: The integration of network analysis and metabolomics provides a scientific basis to propel the clinical use of WZYT for GUs. Our study provides a theoretical basis for the use of Wuzhuyu decoction in the treatment of gastric ulcers.

The human pathogen Helicobacter pylori is a major risk factor for gastric disease development. Serine protease HtrA is an important bacterial virulence factor that cleaves the cell junction proteins occludin, claudin-8 and E-cadherin, which causes gastric tissue damage. Using casein zymography, we discovered that HtrA trimer stability varies in clinical H. pylori strains. Subsequent sequence analyses revealed that HtrA trimer stability correlated with the presence of leucine or serine residue at position 171. The importance of these amino acids in determining trimer stability was confirmed by leucine-to-serine swapping experiments using isogenic H. pylori mutant strains as well as recombinant HtrA proteins. In addition, this sequence position displays a high sequence variability among various bacterial species, but generally exhibits a preference for hydrophilic amino acids. This natural L/S171 polymorphism in H. pylori may affect the protease activity of HtrA during infection, which could be of clinical importance and may determine gastric disease development.

BackgroundHelicobacter pylori is a key agent for causing gastric complications linked with gastric disorders. In response to infection, host cells stimulate autophagy to maintain cellular homeostasis. However, H. pylori have evolved the ability to usurp the host’s autophagic machinery. High mobility group box1 (HMGB1), an alarmin molecule is a regulator of autophagy and its expression is augmented during infection and gastric cancer. Therefore, this study aims to explore the role of glycyrrhizin (a known inhibitor of HMGB1) in autophagy during H. pylori infection.Main methodsHuman gastric cancer (AGS) cells were infected with the H. pylori SS1 strain and further treatment was done with glycyrrhizin. Western blot was used to examine the expression of autophagy proteins. Autophagy and lysosomal activity were monitored by fluorescence assays. A knockdown of HMGB1 was performed to verify the effect of glycyrrhizin. H. pylori infection in in vivo mice model was established and the effect of glycyrrhizin treatment was studied.ResultsThe autophagy-lysosomal pathway was impaired due to an increase in lysosomal membrane permeabilization during H. pylori infection in AGS cells. Subsequently, glycyrrhizin treatment restored the lysosomal membrane integrity. The recovered lysosomal function enhanced autolysosome formation and concomitantly attenuated the intracellular H. pylori growth by eliminating the pathogenic niche. Additionally, glycyrrhizin treatment inhibited inflammation and improved gastric tissue damage in mice.ConclusionThis study showed that inhibiting HMGB1 restored lysosomal activity to ameliorate H. pylori infection. It also demonstrated the potential of glycyrrhizin as an antibacterial agent to address the problem of antimicrobial resistance.

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.

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To study the effect of Jiawei Huangqi Guizhi Decoction on gastrointestinal hormones and TGF-β3 signal pathways in rats with chronic atrophic gastritis (CAG). The model was created by methylnitrosoguanidine (MNNG) comprehensive method. After successful modeling, it was divided into three groups: model group (MC group), frolic acid group (AC group), modified Huangqi Guizhi Decoction high dose group (HH group), modified Huangqi Guizhi Decoction middle dose group (HM group), and modified Huangqi Guizhi Decoction low dose group (HL group). Gastric pathology was observed by HE staining. The levels of gastrin (GAS) and motilin (MTL) in rat serum were detected by ELISA assay. After HE staining, the histopathological sections were analyzed. Inflammatory factors infiltration and disorder of mucosal epithelial cells were found in the model group, which were improved to some extent after administration. According to the pathological chart analysis and score of rats in each group, compared with the model group, the gastric tissue damage of rats in each administration group has been improved in different degrees, among which the pathological scores of HH and HM groups were lower, and the corresponding damage degree was smaller. According to the test results of ELISA, Jiawei Huangqi Guizhi Decoction could reduce the contents of GAS, TGF-β3, and increase MTL abundance in the serum of rats, thus accelerating the apoptosis of tumor cells and inhibiting cancer. Jiawei Huangqi Guizhi Decoction played a positive role in preventing the occurrence of gastric cancer through reducing the concentrations of GAS and TGF-β3 in serum, and increasing the concentration of MLT in serum. This results provided a new treatment idea for CAG.

Antarctic krill oil (KO) prepared using supercritical carbon dioxide extraction and characterized using gas chromatography-mass spectrometry was used to investigate its preventive effect on ethanol-induced gastric tissue damage in a rat model in vivo. KO characterization showed that 74.96% of the unsaturated fatty acids consist of oleic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Rats pre-treated with KO (100, 200, and 500 mg/kg) showed mitigated oxidative stress through enhanced antioxidant enzyme superoxide dismutase (SOD) and reducing enzymes malondialdehyde (MDA) and myeloperoxidase (MPO) in gastric mucosal injury induced by ethanol. Additionally, the secretion of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), the expression of the IκBα/NF-κB signaling pathway, and nitric oxide (NO) production was suppressed. The results also demonstrated a significant decrease in histological injury and hemorrhage scores in a dose-dependent manner in the KO range. Therefore, KO has potential as a food supplement to alleviate ethanol-induced acute gastric mucosal injury.

Eucommia ulmoides leaves are widely developed as food and medicines in China and Japan. Its main components have anti-inflammatory properties against gastric ulcers. The purpose of this study was to assess the protective role of an extract derived from the active components of Eucommia ulmoides leaves (EUL 50) against a gastric ulcer and analyze the underlying antiulcer mechanism. The main components of EUL 50 were identified using an ultra-performance liquid chromatography (UPLC) method. Network pharmacology and molecular docking were performed to predict the possible mechanism of action of EUL 50 in the treatment of gastric ulcers. The rats received EUL 50 intragastric administration twice a day for 3 days. Hydrochloric acid/ethanol (HCl/EtOH) was utilized to induce gastric ulcers, followed by histopathological and histochemical evaluation of the ulcer tissues and determination of the main oxidative stress parameters and inflammatory cytokines. The expression of PI3K/Akt/NF-κB pathway-related proteins was measured. Neochlorogenic acid, chlorogenic acid, rutin, and so on were identified as the major components of EUL 50 by UPLC. The prediction results identified the PI3K/Akt/NF-κB signaling pathway as the main possible protective mechanism against gastric ulcers. Furthermore, in a dose-dependent manner, EUL 50 reduced gastric tissue damage. In addition, the high dose of EUL 50 administration resulted in remarkable reductions in the levels of malondialdehyde (MDA), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and interleukin-1β (IL-1β) by 22.64%, 42.61%, 57.78%, and 56.51%, respectively, and suppression of the phosphorylation of Akt, p65, IKKα, and IκBα by 60.87%, 67.65, 74.58%, and 59.57%, respectively, and increased the antioxidant enzyme activity. EUL 50 is rich in flavonoids and organic acids that can act on the PI3K/Akt/NF-κB signaling pathway; as a result, oxidative stress and inflammation are considerably reduced, and gastric ulcers caused by HCl/EtOH are reduced. PRACTICAL APPLICATION: As a medicinal and food substance, Eucommia ulmoides leaves are widely used in the development of health products. EUL 50, a moderately polar part of E. ulmoides leaves, was obtained by extraction and enrichment and was found to have a better protective effect against HCl/EtOH-induced gastric ulcers. This finding can enrich the traditional application of E. ulmoides leaves and provide a basis for their health product development.

Inhibition of the Akt/NF-κB pathway is involved in the anti-gastritis effects of an ethanolic extract of the rhizome of Atractylodes macrocephala

Likewise other stress response noise stress is also affects the homeostasis of the biological systems and produce stress response in the form of Corticosterone to prevent the damage but if the exposure is longer with higher magnitude it may disrupt the robust ability of the homeostasis and could produce the damage to the biological systems. The goal of our study was to see how five different noise intensities affected stomach tissue damage. 42 healthy rats were divided into five different stress exposure group, normal control (NC) and sham control (SC) groups. Noise stress exposure was delivered for 1 hour per day continued for 30 days in all five noise exposed groups by specially designed noise chamber whereas sham control group of animals kept in noise chamber for 1 hour per day continued for 30 days without noise stress exposure and control group of animals neither exposed to noise stress of any intensities and nor kept in noise chamber without noise but remain in the same experimental room in their homecage for 30 days respectively. Results of the study showed that animals exposed to 60 and 80 dB noise give habituated and not significant Corticosterone, Gastrin and Endothelin-1 responses compared to NC and SC groups while animals exposed to 100, 120 and 140 dB had significantly higher Corticosterone, Gastrin and Endothelin-1 response and also chronic gastric damage was observed compared to later two noise exposed groups respectively. Study concluded that not only higher but also lower noise intensities also initiated the gastric damage even after the adaptation.