Gastric Mucosal Repair Research Articles

Identification of peptides from Corneum Galli Gigeri Endothelium and inhibiting H2O2-induced gastric mucosa associated with the Rho signaling pathway

Corneum Galli Gigeri Endothelium (CGGE) is a traditional food material known for its stomach-strengthening and digestive-enhancing functions. However, the mechanism by which CGGE peptides in repairing gastric mucosal damage is still unclear. In this study, we isolated the B1 component from CGGE peptides and demonstrated its significant activity in repairing gastric mucosal injuries. This component is primarily composed of six peptide segments, namely DYPELS, LPPLEH, SFYYGK, DDDGVGF, VVLPR, and LPYPR. Notably, LPPLEH and LPYPR exhibited effective scratch repair abilities. Furthermore, we elucidated the mechanism underlying the protection of gastric mucosal damage by the B1 component using hydrogen peroxide (H2O2)-induced damage in GES-1 cells.The results showed that the B1 component significantly downregulated the secretion of lactate dehydrogenase (LDH) and malondialdehyde (MDA) in GES-1 cells induced by H2O2 injury (P < 0.05), increased the enzyme activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and significantly increased the synthesis of glutathione (GSH), epidermal growth factor (EGF), transforming growth factor (TGF), hepatocyte growth factor (HGF), trefoil factor (TFF), and vascular endothelial growth factor (VEGF) (P < 0.05). Furthermore, the B1 component significantly upregulated the protein expression of recombinant cell division cycle protein 42 (Cdc42), Rac1, and RhoA in a concentration-dependent manner (P < 0.01). The findings demonstrate that the B1 component has a significant effect on repairing gastric mucosal damage, possibly by improving antioxidant activity and being associated with the Rho signaling pathway. This study provides experimental data and theoretical support for the clinical challenge of gastric mucosal injury repair.

A Rapid Self-Assembling Peptide Hydrogel for Delivery of TFF3 to Promote Gastric Mucosal Injury Repair.

Self-assembled peptide-based nanobiomaterials exhibit promising prospects for drug delivery applications owing to their commendable biocompatibility and biodegradability, facile tissue uptake and utilization, and minimal or negligible unexpected toxicity. TFF3 is an active peptide autonomously secreted by gastric mucosal cells, possessing multiple biological functions. It acts on the surface of the gastric mucosa, facilitating the repair process of gastric mucosal damage. However, when used as a drug, TFF3 faces significant challenges, including short retention time in the gastric mucosal cavity and deactivation due to degradation by stomach acid. In response to this challenge, we developed a self-assembled short peptide hydrogel, Rqdl10, designed as a delivery vehicle for TFF3. Our investigation encompasses an assessment of its properties, biocompatibility, controlled release of TFF3, and the mechanism underlying the promotion of gastric mucosal injury repair. Congo red/aniline blue staining revealed that Rqdl10 promptly self-assembled in PBS, forming hydrogels. Circular dichroism spectra indicated the presence of a stable β-sheet secondary structure in the Rqdl10 hydrogel. Cryo-scanning electron microscopy and atomic force microscopy observations demonstrated that the Rqdl10 formed vesicle-like structures in the PBS, which were interconnected to construct a three-dimensional nanostructure. Moreover, the Rqdl10 hydrogel exhibited outstanding biocompatibility and could sustainably and slowly release TFF3. The utilization of the Rqdl10 hydrogel as a carrier for TFF3 substantially augmented its proliferative and migratory capabilities, while concurrently bolstering its anti-inflammatory and anti-apoptotic attributes following gastric mucosal injury. Our findings underscore the immense potential of the self-assembled peptide hydrogel Rqdl10 for biomedical applications, promising significant contributions to healthcare science.

Construction of Magnolol Nanoparticles for Alleviation of Ethanol-Induced Acute Gastric Injury.

Ethanol (EtOH) has been identified as a potential pathogenic factor in gastric ulcer development primarily due to its association with gastric injury and excessive production of reactive oxygen species. Magnolol (Mag), the principal active compound in Magnolia officinalis extract, is well studied for its notable anti-inflammatory and antioxidant properties. However, its limited solubility, propensity for agglomeration, and low absorption and utilization rates significantly restrict its therapeutic use. This study aims to overcome these challenges by developing a Mag nanoparticle system targeting the treatment and prevention of EtOH-induced gastric ulcers in mice. Utilizing a click chemistry approach, we successfully synthesized this system by reacting thiolated bovine serum albumin (BSA·SH) with Mag. The in vitro analysis revealed effective uptake of the BSA·SH-Mag nanoparticle system by human gastric epithelial cells (GES-1), showcasing its antioxidant and anti-inflammatory capabilities. Additionally, BSA·SH-Mag exhibited gradual disintegration and release in simulated gastric fluid, resulting in a notable reduction of oxidative stress in gastric tissues and mucosal tissue repair and effectively reducing inflammatory expression. Furthermore, BSA·SH-Mag attenuated EtOH-induced gastric inflammation by decreasing the level of NOX4 protein expression and augmenting the level of Nrf2 protein expression. In conclusion, our findings indicate that BSA·SH-Mag represents a promising candidate as an oral therapeutic for gastric ulcer treatment.

To Explore the Mechanism of Periplaneta americana Extracts and Rebeprazole Intervention in Gastric Mucosal Injury Based on ERS Pathway

The mechanism of Periplaneta americana extracts and rabeprazole in treating gastric mucosal injury were explored through ER stress pathway. Acute gastric mucosal injury model rats were made by intragastric administration of anhydrous ethanol. The rats were then randomly assigned to different groups: model group, Periplaneta americana extracts group, rabeprazole group and combined drug group of rabeprazole and Periplaneta americana extracts, with 6 rats in each group. A normal control group, comprising of six rats, was fed a standard diet. Drug groups were treated with intragastric administration for 3 days. The apparent morphological changes of gastric mucosal injury repair in each group of rats were observed. The length and width of the damaged erosion bands were measured and recorded by vernier caliper, and the index of gastric mucosal damage of rats was calculated using the Guth 57 standard method. Pathological repair of gastric mucosal damage was visualized using hematoxylin-eosin staining (HE). The protein expression of gastric mucosa glucose regulated protein (GRP 78), transcriptional activator 6 (ATF 6), C/EBP (CHOP) and interleukin-6 (IL-6) by protein immunoblot (Western Blot, WB). The content of prostaglandin 2 (PGE 2) in the gastric mucosa and serum was observed by an enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC). The results were compared between the other groups and the model group. Intervention treatment in each experimental group demonstrated effective improvement of gastric mucosal injury, reduction in the index of gastric mucosal injury, downregulation of the protein expression of GRP 78, ATF 6, CHOP, and IL-6 in the gastric mucosa. Increasing the content of PGE2 in gastric mucosa and serum, and promoting the repair of inflammation. Notably, the combined drug group exhibited the most significant intervention effect, with a statistically significant difference (P &gt; 0.05). Periplaneta americana extracts, Rabeprazole alone and in combination have different degrees of protection and repair effect on gastric mucosal injury. The regulation of endoplasmic reticulum stress (ERS) may affect the mechanism of action, reducing the protein expression of inflammatory factors, increasing the expression level of PGE2, and promoting the recovery of normal physiological metabolic environment of gastric mucosa.

Treatment of Chronic Gastritis with Traditional Chinese Medicine: Pharmacological Activities and Mechanisms.

Chronic gastritis (CG) is a common clinical digestive system disease, which is not easyily cured and is prone to recurrence. Traditional Chinese medicine (TCM) plays a significant role in the treatment of CG and has attracted increasing attention for clinical applications. In recent years, a large number of reports have shown that TCM has good therapeutic effect on CG. The aim of this paper is to investigate the pharmacological activities and mechanism of action of TCM in the treatment of CAG. Therefore, by searching the databases of Pubmed, China National Knowledge Infrastructure, Wanfang, and Baidu academic databases, this paper has summarized the molecular mechanisms of TCM in improving CG. The results show that the improvement of GC by TCM is closely related to a variety of molecular mechanisms, including the inhibition of Helicobacter pylori (Hp) infection, alleviation of oxidative stress, improvement of gastric function, repair of gastric mucosa, inhibition of inflammatory response, and apoptosis. More importantly, IRF8-IFN-γ, IL-4-STAT6, Hedgehog, pERK1/2, MAPK, PI3K-Akt, NF-κB, TNFR-c-Src-ERK1/2-c-Fos, Nrf2/HO-1, and HIF-1α/VEGF signaling pathways are considered as important molecular targets for TCM in the treatment of GC. These important findings will provide a direction and a basis for further exploring the pathogenesis of GC and tapping the potential of TCM in clinical treatment. This review also puts forward a bright prospect for future research of TCM in the treatment of CG.

Research and Development of a New Sustainable Functional Food under the Scope of Nutrivigilance

Background: The New Global Economy is represented by a series of major features, such as the use of green energy, the reduction of the carbon footprint in all industrial and civil fields, as well as finding alternative food resources. Our main objective was the research of a sustainable food product with a special nutritional purpose in the vision of nutrivigilance, developed in Romania, as an adjuvant in the repair of gastric mucosa. Methods: The materials used in the research and development of the new food are the following: inulin, lactoferrin, sericin, and sodium bicarbonate. The new adjuvant food product in the repair of the gastric mucosa was added to certain foods in order to prevent the patients from being satiated by a single food from a sensory point of view. The resulting food products were organoleptically and physico-chemically analyzed. Results: The new food is sustainable and has versatile uses. It can be hydrated with water, non-carbonated drinks, mixed with cottage cheese, or with fruit puree and oatmeal. It is stable under normal storage conditions and microbiologically safe. Conclusions: Through its versatile use, the new food product for special nutritional conditions represents a worldwide novelty. Through the development of forestry for the cultivation of white or black mulberry (Morus alba and Morus nigra), the raising of silkworms (Bombyx mori), the processing of fibroin to obtain natural silk and the processing of sericin resulting as a residue in the textile industry, the new food product developed actively contribute to the global economy II.

Potential effect of Raw Honey on Gastric Mucosal Healing in Aspirin-induced Rats

Background: Raw honey is a natural ingredient which has a variety of nutrients that can be used for alternative treatments for peptic ulcer disease. This study was carried out to examine the antiulcer effects of Raw Honey against Aspirin induced gastritis in rats. Methodology: Wistar rats were separated into 6 groups. Aspirin suspension 200mg/kgBW was given orally to groups 2-6 for 2 days. Then, group 1 and 2 received carboxymethylcellulose (CMC), groups 3-5 were orally forced-fed with 3.5, 7, and 14mL/kgBW of raw honey, and group 6 received 100mg/kgBW Cimetidine. The tested animals were killed after receiving therapy for 15 days and the gastric mucosa was observed macroscopically of the ulcer index and microscopically through histopathological preparations. The antioxidant effect of raw honey was identified from the lipid peroxidation marker (MDA). Conclusion : Treatment with 7 and 14 ml/kgBW of raw honey promotes gastric mucosal repair based on the macroscopic and microscopic observations. Significant decreases in the levels of the lipid peroxidation marker (MDA) was observed. Significance was defined as p&lt;0.05 compared to the ulcer control group (Group 6).

Effects of Lactobacillus plantarum IS-10506 on gastric protective mucosal factors: an ibuprofen-induced gastric mucosal injury

Background: Gastric mucosal protective factor plays an important roles in gastric homeostasis between mucosal injury and mucosal repair. Previous study implicated probiotics in the repair of the intestinal mucosa, while probiotic role in gastric mucosa remains poorly understood. This study aims to determine the role of probiotic L. plantarum IS-10506 in gastric protective mucosal factors by examining the expression of cyclooxygenase-1 (COX-1), COX-2, prostaglandin E2 (PGE2), and gastric mucus production (Mucin 5AC/ MUC5AC) by surface mucous cells as gastric mucosal protective factors. Methods: Twenty-seven male Wistar rats (Rattus norwegicus) were divided into 3 groups, ie. control, curative and preventive group. Ibuprofen 300mg/kgBW were given to all groups to induce gastric injury, while Lactobacillus plantarum IS-10506 1x109 CFU/day were given into the curative (5 days) and preventive (12 days) groups. Antrum tissue with primary monoclonal antibodies againts COX-1, COX-2, PGE2, and MUC5AC were examined in the day -1, -3, and -5 after necropsy. Results: Number of cells expressed COX-1, COX-2, PGE2 and MUC5AC in curative and preventive groups were significantly higher than control group. L. plantarum IS-10506 showed its efficacy in gastric mucosal repair on third day in the curative group and on first day in the preventive group. L. plantarum IS-10506 probiotic plays a role in gastric protective mucosal factors by promoting cell expression of COX-1, PGE2, and MUC5AC. In addition, it has been determined that L. plantarum IS-10506 inhibits COX-2 expression, that may lead to minimalize the inflammatory conditions and a deterioration of the gastric mucosal environment. Conclusion: Lactobacillus plantarum IS-10506 can prevent ibuprofen-induced antral mucosal damage through gastric protective mucosal factors.

Effect of electroacupuncture on the repair of stress ulcer injury in neurocritical patients: A randomized clinical trial.

Stress ulcer (SU) is one of the main causes of prolonged hospital stay, poor prognosis, and increased mortality in critically ill patients. This study aimed to investigate the effect of electroacupuncture (EA) on SU in patients with severe neurological diseases and explore its possible mechanisms. Taking patients with SU in adult neurocritical care as the research object, they were randomly divided into the EA group and the control group. Through the perioperative EA intervention, the following indicators were documented: main observation indicator (the effective rate of SU treatment), secondary observation indicators (gastric juice pH, gastric juice occult blood test, and stool occult blood test), related mechanisms [repair factors trefoil factor family 2 (TFF2), vascular endothelial growth factor (VEGF), and heat shock protein 70 (HSP70)], complications during hospitalization, and intensive care unit (ICU) stay time. Compared with the control treatment, EA increased the effective rate of SU treatment (85.4% for the EA group, 57.5% for the control group, risk difference: 27.9% (95% CI: 8.3%-45.1%); P < 0.01). EA increased the success rate of gastric juice pH treatment on days 1, 2, and 3 (P < 0.01 for day 1, P < 0.05 for days 2 and 3). EA lowered the positive rate of gastric occult blood test on days 1 and 3 (all P-values < 0.05) and the positive rate of fecal occult blood test on day 3 (P < 0.05). EA also reduced the ICU stay time (P < 0.01) and total hospitalization time (P < 0.05). Compared with day 0, all serum repair factors (VEGF, HSP70, and TFF2) of both groups significantly increased on days 1, 3, and 5 (all P-values < 0.01). Compared with the control group, VEGF in the EA group was increased on days 3 and 5 (all P-values < 0.01); HSP70 was increased on days 1, 3, and 5 (P < 0.05 for day 1, P < 0.01 for days 3 and 5); and TFF2 was increased on days 1, 3, and 5 (all P-values < 0.01). Electroacupuncture promoted the repair of SU damage in severe neurological disease, and its effect was related to enhancing the expression of gastric mucosal repair factors. [https://www.chictr.org.cn/showprojen.aspx?proj=127012], identifier [ChiCTR2100046701].

Preventive and therapeutic effect of Lactobacillus paracasei ZFM54 on Helicobacter pylori-induced gastritis by ameliorating inflammation and restoring gastric microbiota in mice model.

Helicobacter pylori is the most prevalent pathogen causing chronic gastritis, gastroduodenal ulcers, and gastric tumors and is asymptomatically present in 50% of the world's population. This research is focused on investigating the effect of Lactobacillus paracasei ZFM 54 (CCTCC NO:2016667) on attenuating H. pylori-induced gastritis. H. pylori ZJC03 isolated from a patient with gastritis harbored the virulence genes of vacA and cagA and was highly resistant to metronidazole (MIC > 256 μg/mL). In vitro analysis revealed that the potential anti-H. pylori characteristics of L. paracasei ZFM54 in terms of 65.57 ± 1.87% survival rate in simulated gastric juices at a pH of 2.0, 69.00 ± 2.73% auto-aggregation, 30.28 ± 2.24% co-aggregation, 70.27 ± 2.23% urease inhibition, and 57.89 ± 1.27% radical scavenging. In H. pylori infectious mice, L. paracasei ZFM54 pre- and post-treatment reduced the levels of malondialdehyde in liver tissues to 0.71 ± 0.04 nmol/mgprot (p < 0.05) and 0.70 ± 0.06 nmol/mgprot (p < 0.05), respectively. Glutathione levels were increased to 1.78 ± 0.02 μmol/gprot (p < 0.05) and 1.76 ± 0.52 μmol/gprot (p < 0.05), respectively. L. paracasei ZFM54 significantly inhibited H. pylori-mediated inflammation observed in gastric mucosal repair and downregulated the mRNA expression of pro-inflammatory cytokines IFN-γ, IL-1β, and IL-6 (p < 0.01). Importantly, L. paracasei ZFM54 increased Firmicutes and Actinobacteriota and decreased the relative abundance of bacterial taxa belonging to Campilobacterota and Proteobacteria. With the preventive and therapeutic administration of L. paracasei ZFM54, significant reductions in the average relative abundance of genera Helicobacter, Muribaculum, Staphylococcus, Lachnospiraceae_NK4A136_group, Prevotellaceae_UCG-001, Alloprevotella, and Oscillibacter were observed compared to infected mice. These findings suggest that L. paracasei ZFM 54 has the potential to protect against H. pylori infection by ameliorating inflammation and restoring the gastric microbiota.

Effect of Probiotic on Repair of Ethanol-induced Gastric Mucosal Erosion in Wistar Rats

Background: Probiotics can increase mucus secretion as a mechanism to improve barrier function and pathogen exclusion. Several Lactobacillus species can increase mucin expression in human intestinal cells. Lactobacillus Plantarum IS-10506 is a probiotic native to Indonesia derived from curd, fermented milk from Sumatra. Research with Lactobacillus Plantarum IS-10506 showed a protective effect as well as a therapeutic effect on intestinal mucosal damage to the ileum. Objective: Analyzing the effect of probiotic Lactobacillus Plantarum IS-10506 on the acceleration of ethanol-induced gastric mucosal erosion regeneration. Method: Experimental research used 48 rats that were fasted and divided into 3 groups those are K1 group control group, group K2 which was treated with ethanol 43%, and group K3 which was treated with ethanol and probiotic Lactobacillus Plantarum IS-10506. Each group was divided into 4 subgroups based on the day of the sacrifice those are days 1, 3, 5, and 7. The treatment of the test animals is done in 7 days. Epithelial defect was measured by using histopathologic scoring by Roger’s Results: The score of Epithelial defect Group K2 was significantly different compared to group K1 (p=0.036), and K3 (p=0.007). The gastric mucosal repair was completed in day 7 in the probiotic group. Conclusion: Probiotic Lactobacillus Plantarum IS-10506 accelerate mucosal repair in etanol induced gastric mucosal injury

ZINC40099027 Promotes Gastric Mucosal Repair in Ongoing Aspirin-Associated Gastric Injury by Activating Focal Adhesion Kinase.

Nonsteroidal anti-inflammatory drugs cause gastric ulcers and gastritis. No drug that treats GI injury directly stimulates mucosal healing. ZINC40099027 (ZN27) activates focal adhesion kinase (FAK) and heals acute indomethacin-induced small bowel injury. We investigated the efficacy of ZN27 in rat and human gastric epithelial cells and ongoing aspirin-associated gastric injury. ZN27 (10 nM) stimulated FAK activation and wound closure in rat and human gastric cell lines. C57BL/6J mice were treated with 300 mg/kg/day aspirin for five days to induce ongoing gastric injury. One day after the initial injury, mice received 900 µg/kg/6 h ZN27, 10 mg/kg/day omeprazole, or 900 µg/kg/6 h ZN27 plus 10 mg/kg/day omeprazole. Like omeprazole, ZN27 reduced gastric injury vs. vehicle controls. ZN27-treated mice displayed better gastric architecture, with thicker mucosa and less hyperemia, inflammation, and submucosal edema, and lost less weight than vehicle controls. Gastric pH, serum creatinine, serum alanine aminotransferase (ALT), and renal and hepatic histology were unaffected by ZN27. Blinded scoring of pFAK-Y-397 immunoreactivity at the edge of ZN27-treated lesions demonstrated increased FAK activation, compared to vehicle-treated lesions, confirming target activation in vivo. These results suggest that ZN27 ameliorates ongoing aspirin-associated gastric mucosal injury by a pathway involving FAK activation. ZN27-derivatives may be useful to promote gastric mucosal repair.

Protective Effect of Ultraviolet C Irradiation on the Gastric Mucosa of Rats with Chronic Gastritis Induced by Physicochemical Stimulations.

Background Chronic gastritis (CG) is a common digestive disease with the highest morbidity among multiple digestive diseases, which seriously lowers the life quality of patients. The pathological alternations of gastric mucosa, and its possible mechanisms have been the focus of CG-related researches. Accumulative basic and clinical evidence has confirmed that ultraviolet C (UVC) is effective in relieving superficial acute infective inflammation, skin and mucous membrane injuries, and ulcers, and promoting wound healing. Objective This study was aimed at investigating the protective effects of UVC on gastric mucosal injury in rats stimulated with physicochemical irritants like ethanol and exploring the mechanisms underlying the protection by UVC against gastric mucosal injury and CG. Methods Fifty Wistar rats were randomly divided into five groups, including Group A (normal), Group B (model), Group C (omeprazole treatment), Group D (intragastric UVC irradiation for 24 s × 2 yields), and Group E (intragastric UVC irradiation for 48 s × 2 yields). Rats in Groups B–E were made CG model by physicochemical stimulations. All rats were sacrificed one week after the 22-week experiment, and gastric tissues were harvested. Histopathological examinations were performed. The activities of superoxide dismutase and catalase as well as the contents of reduced glutathione and malondialdehyde in gastric mucosal tissues were detected. Serum interleukin-6, interleukin-1beta, tumor necrosis factor-alpha, pepsin, and gastrin were measured. Results Results showed that physiochemical irritants like ethanol could be used for easily establishing a rat CG model that shared similar pathological features with human CG. Intragastric UVC irradiation could promote the repair of gastric mucosa and improve the atrophy of gastric mucosa by inhibiting the inflammatory factors, increasing the levels of pepsin and gastrin, decreasing the expression of lipid peroxide, and enhancing the activity of superoxide dismutase and catalase and the levels of reduced glutathione. UVC irradiation for 48 s × 2 yields showed the strongest protective effect. Conclusion UVC irradiation could inhibit the inflammatory factors, activate the antioxidative system, and enhance the secretion of pepsin and gastrin, which promoted the repair of injured gastric mucosa and improved gastric mucosa atrophy.

Short-chain fatty acid butyrate: A novel shield against chronic gastric ulcer.

Butyrate is one of the most abundant short-chain fatty acids produced by intestinal bacteria. In the present study, the action of butyrate on chronic gastric mucosa lesions was investigated, as well as its underlying mechanism in mice. Male mice from the Institute of Cancer Research were randomly divided into three groups: Sham, model and butyrate groups. Butyrate was administered intragastrically for 7 days to butyrate group mice following the establishment of a gastric ulcer model. Hematoxylin and eosin staining, immunohistochemical analysis, enzyme-linked immunosorbent assay and quantitative polymerase chain reaction were used to determine the therapeutic effects and molecular mechanism of butyrate treatment. The findings demonstrated that butyrate induced a marked shift in superoxide dismutase and catalase activities, along with a decrease in malondialdehyde levels, thereby attenuating oxidative stress. Furthermore, butyrate decreased the levels of pro-inflammatory cytokines interleukin-1β, tumour necrosis factor-α and leukotriene B4, which helped combat inflammatory responses. Moreover, butyrate treatment exerted remarkable positive influences that mediate an increase in 6-keto-PGF-1α (a degradation product of prostacyclin), trefoil factor 2, MUC5AC and fibroblast growth factor-7 levels to promote gastric mucosal repair. The expression of specific receptor GPR109A for butyrate was upregulated, with no significant difference noted in the expression of GPR43 or GPR41. Overall, the present findings revealed that butyrate exerted therapeutic effects by upregulating mucosal repair factors and stimulating protective responses against oxidation and inflammation. GPR109A may be the key receptor for butyrate therapy.

Molecular Alterations in the Stomach of Tff1-Deficient Mice: Early Steps in Antral Carcinogenesis.

TFF1 is a peptide of the gastric mucosa co-secreted with the mucin MUC5AC. It plays a key role in gastric mucosal protection and repair. Tff1-deficient (Tff1KO) mice obligatorily develop antropyloric adenoma and about 30% progress to carcinomas. Thus, these mice represent a model for gastric tumorigenesis. Here, we compared the expression of selected genes in Tff1KO mice and the corresponding wild-type animals (RT-PCR analyses). Furthermore, we systematically investigated the different molecular forms of Tff1 and its heterodimer partner gastrokine-2 (Gkn2) in the stomach (Western blot analyses). As a hallmark, a large portion of murine Tff1 occurs in a monomeric form. This is unexpected because of its odd number of seven cysteine residues. Probably the three conserved acid amino acid residues (EEE) flanking the 7th cysteine residue allow monomeric secretion. As a consequence, the free thiol of monomeric Tff1 could have a protective scavenger function, e.g., for reactive oxygen/nitrogen species. Furthermore, a minor subset of Tff1 forms a disulfide-linked heterodimer with IgG Fc binding protein (Fcgbp). Of special note, in Tff1KO animals a homodimeric form of Gkn2 was observed. In addition, Tff1KO animals showed strongly reduced Tff2 transcript and protein levels, which might explain their increased sensitivity to Helicobacter pylori infection.

Use of medicinal plants for the treatment of gastric ulcer in some parts of Southwestern Nigeria

Ulcer is erosion in the lining of the stomach or duodenum. It is caused by disruption of the gastric mucosal defense and repair systems. There has been much interest in natural medicines derived from traditional knowledge of pharmacological properties of plants recently. The major aim of this study was to conduct an ethnobotanical survey of plants used in the treatment of Gastric ulcers in some local government areas of Ibadan, South-West, Nigeria. Five local government areas which have prominent traditional medical practitioners and herbal markets were visited. Ninety-two plants belonging to forty-five different families were recorded. The prominent plants’ families recorded include; Apocynaceae, Loranthaceae, and Lamiaceae. Some of the most frequently used medicinal plants mentioned by the respondents are: Sphenocentrum jollyanum Pierre, Euadenia trifoliolata (Sch. &Thon.) Oliv., Khaya ivorensis A. Chev., Lonchocarpus cyanescens Benth, and Kigelia africana (Lam.) Benth. Most of the herbs were prescribed together with other plants and recipes. Modes of administration were mostly concoctions and decoctions. Cultivation and proper documentation of some of the plants which may become endangered over time is therefore encouraged. Most of the identified plants have been used regularly by the traditional medical practitioners and the efficacies have been proven. Key words: Gastric ulcer, ethnobotanical survey, medicinal plants, traditional medicine, South-west Nigeria.

Effects of different doses of ginger-partitioned moxibustion on trefoil factor 1, mucin 5AC and epidermal growth factor receptor in rats with spleen deficiency syndrome

To observe the effects of different doses of ginger-partitioned moxibustion on serum trefoil factor 1 (TFF1) and mucin 5AC (MUC5AC) levels, as well as the expression of epidermal growth factor receptor (EGFR) in gastric mucosa of rats with spleen deficiency syndrome, therefore, to explore the possible mechanism and the dose-effect characteristics of ginger-partitioned moxibustion in spleen deficiency syndrome. Seventy-five SPF grade Sprague-Dawley (SD) rats were randomly divided into a blank control group (group A), a model group (group B), a 3 moxa-cone ginger-partitioned moxibustion group (group C1), a 6 moxa-cone ginger-partitioned moxibustion group (group C2) and a 9 moxa-cone ginger-partitioned moxibustion group (group C3) using random number table method, 15 rats in each group. Except group A, rats in the other groups received intragastric administration of 4 °C 200% concentrated Da Huang (Radix et Rhizoma Rhei) to prepare spleen deficiency syndrome model. After successful modeling, rats in group B received no treatment; rats in group C1, C2 and C3 were treated with 3, 6 and 9 moxa-cone ginger-partitioned moxibustion at Zusanli (ST 36) and Zhongwan (CV 12) respectively for 8 continuous days. The general symptom score of rats was observed. The serum levels of TFF1 and MUC5AC were detected by enzyme-linked immunosorbent assay (ELISA). The expression of EGFR protein in gastric mucosa was detected by immunohistochemistry. After the treatment, compared with group A, the spleen deficiency symptom score was increased in group B, the levels of serum TFF1 and MUC5AC, the EGFR protein expression in gastric tissues of group C1, C2 and C3 were significantly increased (all P 0.05). The mechanism may be related to the increase of serum TFF1 and MUC5AC levels and activation of EGFR protein. Ginger-partitioned moxibustion can improve the symptoms, as well as promote the proliferation and repair of gastric mucosa in rats with spleen deficiency. The therapeutic efficacy of 6 or 9 moxa-cone ginger-partitioned moxibustion is better than that of 3 moxa-cone ginger-partitioned moxibustion, while the efficacies are equivalent between 6 and 9 moxa-cone ginger-partitioned moxibustion groups.

Novel approach to gastric mucosal defect repair using fresh amniotic membrane allograft in dogs (experimental study)

BackgroundGastric mucosal defect could result from several causative factors including the use of nonsteroidal anti-inflammatory drugs, Helicobacter pylori infection, gastrointestinal and spinal cord diseases, and neoplasia. This study was performed to achieve a novel simple, inexpensive, and effective surgical technique for the repair of gastric mucosal defect.MethodsSix adult male mongrel dogs were divided into two groups (three dogs each). In the control positive group (C + ve), dogs were subjected to surgical induction of gastric mucosal defect and then treated using traditional medicinal treatment for such a condition. In the amniotic membrane (AM) group, dogs were subjected to the same operation and then fresh AM allograft was applied. Clinical, endoscopic, biochemical (serum protein and lipid and pepsin activity in gastric juice), histopathological, and immunohistochemistry evaluations were performed.ResultsRegarding endoscopic examination, there was no sign of inflammatory reaction around the grafted area in the AM group compared to the C + ve group. The leukocytic infiltration in the gastric ulcer was well detected in the control group and was less observed in the AM group. In the AM group, the concentrations of both protein and lipid profiles were nearly the same as those in serum samples taken preoperatively at zero time, which indicated that the AM grafting acted the same as gastric mucosa. The re-epithelization of the gastric ulcer in the C + ve group was not yet detected at 21 days, while in the AM group it was well observed covering most of the gastric ulcer. AM accelerated the re-epithelization of the gastric ulcer. The fibrous connective tissue and the precursor of collagen (COL IA1) were poorly detected in the gastric ulcer with AM application.ConclusionUsing fresh AM allograft for repairing gastric mucosal defect in dogs showed great impact as a novel method to achieve optimum reconstruction of the gastric mucosal architecture and restoration of pre-epithelial, epithelial, and post-epithelial normal gastric mucosal barriers.

Effect of herbal cake-partitioned moxibustion on MEK1/2 and ERK1/2 expressions of gastric tissues in rats with spleen deficiency syndrome

To observe the effect of herbal cake-partitioned moxibustion on the expressions of mitogen-activated protein kinase (MEK1/2) and extracellular regulatory protein kinase (ERK1/2) in gastric tissues of rats with spleen deficiency syndrome, and to explore the possible mechanisms of herbal cake-partitioned moxibustion in treating spleen deficiency syndrome. Sixty Sprague-Dawley (SD) rats were randomly divided into a blank control group (group A), a model group (group B), a ranitidine group (group C), and a herbal cake-partitioned moxibustion group (group D) by random digit, 15 rats in each group. Rat models of spleen deficiency syndrome were made by intragastric administration of 4 °C 200% concentrated Da Huang (Radix et Rhizoma Rhei). After successful modeling, the rats in group C were treated with 25 mg/(kg·bw) ranitidine by intragastric adminstration and rats in group D were treated with herbal cake-partitioned moxibustion at Zusanli (ST 36) and Zhongwan (CV 12), for 8 d. Excepted for rats in group A, all the other rats were treated with indomethacin at 5 mg/(kg·bw) at 8:00 a.m. on the second day after finishing all the intervention and sacrificed 7 h later to isolate the stomach. Histopathological changes of the gastric tissues were observed under light microscope after hematoxylin-eosin (HE) staining. The protein expressions of MEK1/2 and ERK1/2 in the gastric tissues were detected by immunohistochemistry. After intervention, the gastric mucosal injury in group B was significantly severer than that in group A, with large breakage and ablating; the damage of gastric mucosa was decreased in group C compared with group B; the gastric mucosal surface remained relatively complete, and the status of breakage and ablating was significantly improved. After intervention, compared with group A, the protein expressions of MEK1/2 and ERK1/2 in gastric tissues of the other groups were significantly higher (P<0.01). Compared with group B, the protein expressions of MEK1/2 and ERK1/2 in group C and D were significantly higher (all P<0.01). Compared with group C, the protein expressions of MEK1/2 and ERK1/2 in group D were significantly higher (P<0.01). Herbal cake-partitioned moxibustion promotes the repair of gastric mucosa in rats with spleen deficiency syndrome, via improving protein expressions of MEK1/2 and ERK1/2 in gastric tissues, as well as activating MEK/ERK signaling pathway.

Possibilities for optimization of eradication therapy for Helicobacter pylori infection in modern clinical practice

A steady decline in the effectiveness of standard eradication therapy (ET) regimens for Helicobacter pylori infection necessitates a search for ways of their optimization, by enhancing the efficiency of treatment protocols and by improving their safety and tolerability. The review systematizes the data available in the literature on main accessible methods for optimizing ET regimens. Among the optimization methods that can considerably enhance the efficiency of ET regimens, one may identify their addition of a bismuth agent (by 10-20%), the use of rebamipide (by 11.9%), adjuvant therapy with probiotics (by 8.1-13%), or double-dose proton pump inhibitors (by 8%). Only adjuvant therapy with probiotics results in a significant decrease in the incidence of side effects from ET. In posteradication period, rebamipide should be used to potentiate gastric mucosal repair and to regress inflammatory processes.