Gastritis In Rats Research Articles

Effects of Sweetgum Oil on Experimental Chronic Gastritis in Rat Model

Background: Sweetgum oil has been traditionally used to treat wounds, respiratory tract problems, osteoarthritis and various stomach ailments. In this study, the effects of sweetgum oil on ethanol-induced chronic gastritis in rats were investigated. Methods: Thirty Wistar albino rats were divided into 5 groups. Group 1 served as control and received no treatment. Except for control, all animals received oral doses of 8 g/kg of 56% ethanol twice a week for 4 weeks to induce gastritis. Group 2, the ethanol group received only ethanol. Group 3 was treated with the conventional treatment of 20 mg/kg omeprazole daily for 2 weeks. Group 4 was treated with 150 mg/kg of sweetgum oil dissolved in olive oil daily for 2 weeks. Group 5 was treated orally with 0.6 ml olive oil daily for 2 weeks. Result: Histopathological and immunohistochemical examinations were performed on the stomach samples. Ethanol caused severe erosive ulcerative lesions in the gastric mucosa and inflammatory cell infiltrations in the propria mucosa. In immunohistochemical examination, marked increases in interleukin-10 (IL-10), interleukin-1β (IL-β) and platelet endothelial cell adhesion molecule 1 (PECAM-1) expressions were observed in this group. Omeprazole treatment significantly reduced these pathological findings. Sweetgum oil provided significant improvement in histopathological and immunohistochemical findings, but the protection was not as effective as omeprazole. Moderate healing effects were also observed with olive oil. Sweetgum oil has a curative effect on chronic gastritis, although it is not as effective as omeprazole. Moreover, olive oil has a curative effect on gastritis.

Gastroprotective Effect of Quercus infectoria Olivier Galls on Ethanol-Induced Gastritis in Rats.

One of the common inflammatory disorders that substantially affects the stomach and its mucosa is gastritis. It can be induced by non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, alcohol, Helicobacter pylori infection, and stress. These factors affect cellular regeneration, mucus production, and bicarbonate secretion, resulting finally in inflammation and ulceration. Ethanol-induced gastritis is one of the commonly used models for studying the pathology of gastritis and investigating the effect of drugs in managing the disease. Several drugs, such as proton pump inhibitors (PPIs), are available to control and correct the pathological signs of gastritis; however, the side effects of such drugs represent an obstacle to their applications in many cases. Quercus infectoria(QI) Olivier galls are formed as a pathological response to wasp insults to the tree. They are rich in several bioactive molecules, e.g., gallotannins that have been shown to be effective in several inflammatory conditions due to their antioxidant and anti-inflammatory potentials. In this study, we aimed to evaluate the therapeutic potential of QI gall extract (QIGE) in treating ethanol-induced gastritis in rats. To test this, 20 adult male Swiss rats were divided into four groups: healthy control, ethanol-treated (80% in water, 5 ml/kg, per oral gavage), ethanol + omeprazole (20 mg/kg, per oral gavage), and ethanol + QIGE (300 mg/kg, per oral gavage). QIGE was administered for seven days before ethanol administration, which took place three hours after the last QIGE dose. Three hours after ethanol intake, animals were euthanized, gastric content was collected, and stomach tissue was examined for macroscopic changes and then fixed to be further utilized for histological assessment by hematoxylin and eosin (H&E), periodic acid-Schiff (PAS), and Masson's trichrome staining. Ethanol treatment significantly decreased gastric pH and increased gastric acidity compared to healthy control. It also induced clear morphological and histological damage and ulceration, depleted mucus on the gastric epithelium, and induced edema and collagen deposition in gastric submucosa. The QIGE treatment ameliorated the changes in gastric pH and total acidity. It also protected stomach tissue from ethanol-induced ulceration, histopathological changes, edema, and collagen deposition. The protective effects of QIGE were comparable to those of omeprazole. In conclusion, QI gall extract possesses a promising gastroprotective effect against ethanol-induced gastritis.

Effects of Desmodium caudatum on Gastrointestinal Hormones and Intestinal Flora in Rats with Gastritis.

In order to preliminarily explore the effects of Desmodium caudatum on gastritis and intestinal flora in rats, a chronic gastritis rat model was established using the classic sodium salicylate method. Eighteen SPF rats were divided into three groups: the control group (Group C), the model group (Group M), and the treatment group (Group T). Pathological sections of the gastric wall were taken from rats in each group. Furthermore, the concentrations of gastrin and malondialdehyde in the serum of rats in each group were determined by ELISA. Additionally, the effects of D. caudatum on the intestinal flora of rats with gastritis were explored through a detailed comparison of gut bacterial communities in the three groups, employing Illumina-based 16S rRNA gene sequencing. The results indicated that D. caudatum decoction could reduce the malondialdehyde content and increase the gastrin content. Moreover, D. caudatum decoction was found to enhance the diversity and abundance of intestinal flora, exerting a positive impact on the treatment of gastritis by regulating and restoring the intestinal flora.

Green synthesis of zinc oxide nanoparticles using ethanolic extract of Gliricidia sepium (Jacq.) Kunth. ex. Walp., stem: Characterizations and their gastroprotective effect on ethanol-induced gastritis in rats

The study presents a significant advancement in drug delivery and therapeutic efficacy through the successful synthesis of Gliricidia sepium(Jacq.) Kunth. ex. Walp., stem zinc oxide nanoparticles(GSS ZnONPs). The phenolic compounds present in Gliricidia sepium stem (GSS) particularly vanillic acid, apegnin-7-O-glucoside, syringic acid, and p-coumaric acid which were identified by HPLC. These compounds shown antioxidant and anti-inflammatory properties. GSS ZnONPs demonstrate pronounced gastroprotective effects against ethanol-induced gastritis, evidenced by the reduction in gastric lesions and mucosal injury upon its treatment. Histopathological evaluation and immunohistochemical analysis of nuclear factor erythroid 2-related factor 2 (Nrf2) expression further validate these results, revealing the amelioration of ethanol-induced gastritis and improved gastric tissue condition due to their treatment. Noteworthy is the dose-dependent response of GSS ZnONPs, showcasing their efficacy even at lower doses against ethanol-induced gastritis which is confirmed by different biomarkers. These findings have substantial implications for mitigating dosage-related adverse effects while preserving therapeutic benefits, offering a more favorable treatment approach. This study aims to investigate the potential gastroprotective activity of GSS ZnONPs against gastritis.

Exploration of the intestinal flora to reveal the important contribution of Radix Astragali to Huangqi Jianzhong Tang in treating chronic atrophic gastritis rats

Radix Astragali (Huangqi in Chinese, HQ) is a commonly used Chinese herbal medicine for thousands of years. In this study, A classic prescription Huangqi Jianzhong tang (HQJZ) was selected to evaluate the important effect of HQ on rats with chronic atrophic gastritis (CAG) from the perspective of intestinal flora in cecal contents samples. Traditional pharmacological indicators, including weight change, pathological examination and biochemical indicators showed that HQ exerted favorable contribution to HQJZ against CAG, where the efficiencies of HQ and HQJZ were better than HY (HQJZ prepared without HQ). An accurate strategy was adopted to screen out the differential metabolites in the metabolomis analysis of intestinal flora in cecal contents samples based on the optimal screening factors, including VIP (importance of variables in projection), FC (fold change), AUROC (area under the receiver operating characteristic curve) and -ln(p-value), which were evaluated based on their interpreting, grouping, and predicting abilities of the performed orthogonal partial least-squares-discriminate analysis (OPLS-DA) models. Ten altered differential metabolites were obtained and associated with the intestinal flora, which HQ exerted the important metabolic contributions to HQJZ. The efficacy on the diversity of intestinal flora and their correlations with the altered metabolites further showed the important role of HQ in HQJZ composition. This work provided valuable approach for looking for potential biomarkers associated with metabolomics research with more accuracy, and provided new insights into the mechanisms to explain the efficacy of HQ contributing to HQJZ formula.

El efecto protector del extracto de Granada contra la úlcera gástrica experimental inducida por etanol en ratas

The Pomegranate (Punica granatum) is a commonly found fruit in the Mediterranean and Iran, which has a variety of uses including medicinal purposes, cosmetics, and as a spice in culinary applications. Pharmacological functions of Pomegranate include antioxidation, anti–tumor, anti–hepatotoxicity, anti–lipoperoxidation and antibacterial properties. The aim of this study was to evaluate the therapeutic efficacy of Pomegranate extract by utilizing its antioxidant activity in an experimental rat model of gastritis induced by ethanol. In the study, 24 female Wistar albino rats (180–200 g) were used. Gastritis in rats was induced using Ethanol. In experimental groups, Tumor necrosis factor–alpha, Myloperoxidase, Superoxide Dismutase and Malondialdehyde were examined for biochemical analyzes. Streptavidin peroxidase immunohistochemistry method was applied to gastric tissues with gastritis. A statistically significant difference was observed between Superoxide Dismutase and Meloperoxidase levels. CD8 and CD68 immunoreactivity was higher in the Ethanol group compared to the other groups. A decrease was observed in CD8 and CD68 positive immunoreactivity in Ethanol+Pomegranate extract group compared to Ethanol group. The study found that the immunoreactivity of MHC–I and MHC–II was found in specific locations, namely intraepithelial lymphocytes located in the epithelium, some capillary vessel endothelium, and connective tissue. Changes in anti–oxidative stress markers such as Superoxide Dismutase and Myloperoxidase contributed to the mucosal protective effect of Pomegranate extract in Ethanol–induced gastritis.

Rumex nervosus nanoparticles versus aqueous extract: introduction of novel immunomodulatory anti-inflammatory nano-preparation for management of paw oedema and gastritis in rats

BackgroundRumex nervosus is abundant in East African and Arabian countries, and is used in curing gastrointestinal diseases as well as in wound healing. The current study intends to assess Rumex nervosus aqueous extract's anti-inflammatory benefits compared to its nanoparticles on rat paw edema and its gastric mucosal protection against ulceration.Materials and methodsIn-vitro cytotoxicity effects and antioxidant activity of Rumex nervosus nanoparticles versus aqueous extract were studied, followed by a pilot in vivo pharmacological study to determine the suitable dose of nanoparticles that would be used in the safety and efficacy studies in comparison with the aqueous extract. Its protective effects on arthritis and soft tissue inflammation were studied in rat paw edema and gastric ulcer models. Rumex nervosus extract (250 and 500 mg/kg) and nanoparticles (3.3 and 6.6 mg/kg) were given to four groups of rats orally before induction of paw oedema with subplantar 0.2 ml (1% w/v) formaldehyde or gastritis with oral ethanol 1 ml (70%), besides negative, positive control and reference groups.ResultsPaw volumes and gastric ulcer indices, as well as the anti-inflammatory and antioxidant parameters (kappa β, Paraoxonase1, and Malondialdehyde) that were measured in sera showed a marked reduction in groups treated with high doses of Rumex nervosus extract, and nanoparticles. Histopathologic and histochemical assessment of the stomachs confirmed the other investigations. All results were significant compared to positive control untreated groups.ConclusionsMost studies demonstrated Rumex nervosus’s protective anti-inflammatory benefits with the superiority of large doses of nanoparticles, offering a promising natural solution for low cost against inflammation.

Integrating metabolomics, 16S rRNA sequencing, network pharmacology, and metorigin to explore the mechanism of Cinnamomi Cortex in treating chronic atrophic gastritis rats

BackgroundCinnamomi cortex called as Rougui (RG) in Chinese was a widely used food-medicine homology. RG has the potential to treat chronic atrophic gastritis (CAG), a disease with widespread impact in the Chinese population. PurposeThis study aimed to explore its mechanism against CAG based on amalgamated strategies. MethodsNetwork pharmacology was used to predict the potential effective components and the core targets of RG against CAG based on the comprehensive chemical characterization using UHPLC-Q/TOF MS (ultra high performance liquid chromatogramphy-quadrupole/time-of-flight mass spectrometry). The CAG animals model were further used to validate its pharmacodynamics, of which gut microbiota of caecal contents were analyzed by integrating metabolomics, 16S rRNA sequencing, Metorigin metabolite traceability analysis and molecular docking to explore its action mechanism. ResultsNetwork pharmacology firstly predicted the efficacy of RG was attributed to four effective components and seven targets. Metabolomics of caecal contents in CAG rats revealed primary bile acid biosynthesis was its targeted metabolic pathway associated with the metabolism of gut microbiota coupled with Metorigin traceability analysis. 16S rRNA sequencing showed that RG treated CAG by regulating the imbalance of gut microbiota. Molecular docking further confirmed that the effective components of RG could intervene with potential targets, metorigin analysis pathway, and key enzymes of gut microbiota metabolic pathways. ConclusionOur results proved that RG exerted favorable effect on CAG. The four active ingredients (quercetin, kaempferol, oleic acid, and (-)-epicatechin) of RG were the key to exert drug effect, which could targeted the core target of CAG, primary bile acid biosynthesis and intestinal flora metabolic pathways.

The protective effect of Aspalathus linearis against the experimental gastric ulcer induced by ethanol in rats

This study aimed to investigate the effect of Aspalathus linearis on the expression levels of major histocompatibility complex (MHC) molecules and their ability to present antigens to CD8, CD68, and T cells in an experimental rat model of gastritis. Furthermore, changes in tumor necrosis factor–alpha (TNF–α), myeloperoxidase, superoxide dismutase, and malondialdehyde levels due to the antioxidant properties of the plant were evaluated. The study included 24 female Wistar albino rats (Rattus norvegicus). A. linearis was administered to the treatment groups of an ethanol–induced gastritis rat model via oral gavage for 5 days the blood and stomach tissues were sampled for analysis. Biochemical evaluation revealed that TNF–α and myeloperoxidase levels decreased and superoxide dismutase activity increased in the A. linearis–treated groups compared with the ethanol–treated group. Histochemical evaluation revealed that the severity of inflammation decreased in the rats with gastritis treated with A. linearis. In addition, the number of cells expressing CD8 and CD68 decreased. The number of MHC–II immunopositive cells was higher in the A. linearis–treated group compared with the control and other treatment groups. A. linearis exhibits a protective effect on gastric mucosa by reducing the severity of oxidative stress owing to its antioxidant, anti–inflammatory, and antiapopitotic properties.

Huangqi Jianzhong Tang treats chronic atrophic gastritis rats by regulating intestinal flora and conjugated bile acid metabolism.

Huangqi Jianzhong Tang (HQJZ) is effective for treating chronic atrophic gastritis (CAG). The present study was carried out to reveal the mechanism of HQJZ in CAG rats. The metabolism and microbial composition of the cecal contents in CAG rats were analyzed through the integration of an untargeted metabolomic approach using ultra-high-performance liquid chromatography coupled with the quadrupole-time of flight mass spectrometry (UHPLC-QTOF-MS) and 16S rRNA gene sequencing, respectively. Finally, MetOrigin analyses were performed to explore the relationship between differential metabolites and intestinal flora. The results showed that HQJZ could significantly regulate metabolic disorders, especially conjugated acid metabolites. 16S rRNA gene sequencing analysis illustrated that HQJZ decreased the abundance of Acetobacter, Desulfovibrio, Escherichia, and Shigella. MetOrigin metabolite traceability analysis showed that the six bile acids associated with HQJZ efficacy included three bacteria-host cometabolites, which were involved in the primary bile acid biosynthesis pathway. Research presented here confirmed that conjugated bile acid metabolism was key to the treatment of CAG by HQJZ and correlates strongly with Bacteroides acidifaciens and Prevotella copri. These findings provide new insights into the mechanisms to explain the efficacy of HQJZ.

Pharmacokinetics and tissue distribution of 12 major active components in normal and chronic gastritis rats after oral administration of Weikangling capsules

Ethnopharmacological relevanceWeikangling Capsules (WKLCs) have been used in the clinic for the treatment of gastrointestinal disorders for more than 30 years. However, the pharmacokinetic characteristics and tissue distribution of its major bioactive components in rats under different physiological and pathological conditions are unclear. Aim of the studyIn this study, we aimed to clarify the differences in pharmacokinetic parameters and tissue distribution of the major active components in WKLCs under physiological and pathological states. Materials and methodNormal and ethanol-induced chronic gastritis rats received 2.16 g/kg WKLCs by gavage, and urine, feces, plasma, and tissue (heart, liver, spleen, lung, kidney, stomach, and small intestine) samples were obtained. The active components in urine, feces and plasma were detected by ultra-high-performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (UHPLC-Q-TOF-MS/MS). A rapid and sensitive analytical method, ultra-high-performance liquid chromatography coupled with triple-quadrupole linear ion-trap tandem mass spectrometry (UHPLC-QTRAP-MS/MS), was established and validated to clarify and compare the pharmacokinetics and tissue distribution of the major active components in normal and chronic gastritis rats. ResultsA total of 36 chemical components in the feces, urine, and plasma of chronic gastritis rats were identified by UHPLC-Q-TOF-MS/MS. Among them, 20 were the prototype components of WKLCs, and 16 were metabolites. The pharmacokinetic characteristics and tissue distribution of 12 prototype components were successfully analyzed by UHPLC-QTRAP-MS/MS. The pharmacokinetic results showed that the Cmax, AUC0-t, and AUC0-∞ of paeoniflorin, glycyrrhizic acid, and glycyrrhetinic acid were distinctly higher than those of the other components in normal and chronic gastritis rats. Compared to normal rats, the Cmax, AUC0-t, and AUC0-∞ of albiflorin, liquiritin apioside, liquiritin, isoliquiritin, ononin, isoliquiritigenin, dactylorhin A, and glycyrrhizic acid were significantly increased in chronic gastritis rats (P < 0.05), while the Cmax, AUC0-t and AUC0-∞ of militarine and liquiritigenin had significantly lower decreases in chronic gastritis rats (P < 0.05). The results of the tissue distribution showed that the 12 components were widely distributed in the heart, liver, spleen, lung, kidney, stomach, and small intestine of rats, of which the liver, kidney, stomach, and small intestine were the main accumulative organs. Compared with normal rats, the concentrations of 12 components in the liver, kidney, stomach, and small intestine of chronic gastritis rats were widely higher than those of normal rats at the same time points. ConclusionThe pharmacokinetic characteristics and tissue distribution of 12 active components of WKLCs were comprehensively characterized and elucidated in normal and chronic gastritis rats. These findings laid a solid foundation for revealing the pharmacodynamic material basis of WKLCs in treating gastrointestinal disorders.

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).

Bile acid metabolism involved into the therapeutic action of Xiaojianzhong Tang via gut microbiota to treat chronic atrophic gastritis in rats

BackgroundAs a classical traditional Chinese medicine (TCM), Xiaojianzhong Tang (XJZ) is effective in treating chronic atrophic gastritis (CAG). However, the pharmacological mechanism of XJZ has not been fully explained. PurposeThe purpose of this study was to investigate the mechanism of XJZ against CAG rats via gut microbiome using a multi-omics approach. MethodsThe rat cecal contents were analyzed through the integration of an untargeted metabolomic approach based on ultra-high performance liquid chromatography coupled with the quadrupole-time of flight mass spectrometry (UHPLC-QTOF-MS) and 16S rRNA gene sequencing. Finally, the interaction of differential metabolites with bile acid (BA)-related targets was verified by molecular docking. ResultsA new strategy was adopted to screen out the differential metabolites based on the comprehensive evaluation of VIP, |log2(FC)|, -ln(p-value) and ǀp(corr)ǀ. As results, XJZ showed favor regulations on the screened metabolites, cholic acid, deoxycholic acid, glycoursodeoxycholic acid, taurochenodesoxycholic acid, docosahexaenoic acid and L-isoleucine. The 16S rRNA gene sequencing analysis showed that XJZ could regulate gut microbiota disturbances in CAG rats, especially bile acid (BA) metabolism-related bacteria (Butyricimonas, Desulfovibrio, Bacteroides, Parabacteroides, Acetobacter and Alistipes). Molecular docking further showed that the differential metabolites regulated by XJZ had a good docking effect on BA-related targets. ConclusionThe current work indicated that XJZ's therapeutic action was strongly linked to BA-related microorganisms and metabolic processes. These findings provided new insights into the effects of XJZ for the treatment of CAG.

Integrated pharmacokinetics of Huangqi Jianzhong Tang in normal and chronic atrophic gastritis rats

Huangqi Jianzhong Tang (HQJZ) is a famous traditional Chinese medicine formula widely used in the treatment of gastrointestinal diseases in China. In this study, an ultra-performance liquid chromatography-mass spectrometry (UHPLC-MS/MS) was used to study the pharmacokinetics of 12 prototypical components and one metabolite in HQJZ in normal and chronic atrophic gastritis rats. The results showed that the area under the concentration-time curve and peak concentration of most flavonoids and flavonoid glycosides were decreased, and the half-life and mean residence time were significantly increased, which indicated that the absorption of drugs in disease was decreased less and for longer in vivo. Then, an integrated pharmacokinetic study was carried out using the pharmacokinetic parameter model integration of each component. The results showed that the absorption of drugs in vivo with disease was reduced, and the absorption speed of flavonoids and flavonoid glycosides was accelerated. This study will provide the basis for the clinical medication safety of HQJZ.

Jian-Pi-Yi-Qi-Fang ameliorates chronic atrophic gastritis in rats through promoting the proliferation and differentiation of gastric stem cells.

BackgroundJian-Pi-Yi-Qi-Fang (JPYQF) is a traditional Chinese medicine (TCM) herbal formula for treating chronic atrophic gastritis (CAG) in the clinic; however, its related mechanism remains unclear. The purpose of this study was to explore the potential mechanisms of JPYQF in treating CAG by examining proteins and genes related to the proliferation and differentiation of gastric stem cells and Wnt signaling.MethodsA CAG model was established in Sprague-Dawley (SD) rats which were induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and ranitidine. We randomly divided 25 CAG rats into 5 groups: the model group, positive drug group, low-dose group of JPYQF (JPYQF-L), middle-dose group of JPYQF (JPYQF-M), and high-dose group of JPYQF (JPYQF-H), with 5 rats of the same age classified into the control group. The body weight of rats was measured and their gastric morphology was visually assessed. Furthermore, pathological analysis of rat gastric tissue was performed. The expression levels of proteins and genes associated with the proliferation and differentiation of gastric stem cells and Wnt signaling were measured via immunohistochemistry and reverse transcription quantitative polymerase chain reaction (RT-qPCR).ResultsCompared with the model group, treatment with JPYQF increased the body weight of the rats, and relieved the gastric atrophy and inflammation. Compared with the control group, the protein and messenger RNA (mRNA) expression levels of gastric stem cell proliferation and differentiation markers Lgr5, Sox2, Ki67, PCNA, Muc5AC, and Wnt signaling initiator Wnt3A and enhancer R-spondin-1 (Rspo1) were decreased in the model group. Treatment with JPYQF increased the protein and mRNA expression levels of these markers.ConclusionsThe Wnt signaling of CAG rats may be in a low activation state, which inhibits the proliferation and differentiation of gastric stem cells, so that gland cells cannot be replenished in time to repair the damaged gastric mucosa. The TCM formula JPYQF could enhance Wnt signaling to promote the restricted proliferation and normal differentiation of gastric stem cells, thereby improving gastric mucosal atrophy in CAG rats, which provides a novel and robust theoretical basis for CAG treatment.

Efficiency evaluation of Amlodipine combined with N-acetylcysteine on Indomethacin-induced gastritis in rats

Introduction: It is a well-known phenomenon that nonsteroidal anti-inflammatory drugs cause gastric mucosal damage. Amlodipine is a third generation dihydropyridine-type calcium channel blocker; it can inhibit inflammatory cytokines and enhance antioxidant defenses. N-acetylcysteine can act both as a precursor of reduced glutathione and as a direct ROS scavenger. Moreover, N-acetylcysteine has been purported to have anti-inflammatory properties.&#x0D; Materials and methods: 34 albino Wistar rats were used. The model of gastritis was induced by subcutaneous Indomethacin prepared in 5% sodium bicarbonate administered at a dose rate of 9 mg/kg for two days at 24h intervals. N-acetylcysteine (500 mg/kg), Amlodipine (10 mg/kg) and N-acetylcysteine (500 mg/kg) combined with Amlodipine (5 mg/kg) were administrated for seven consecutive days beginning 24 h after the first Indomethacin injection. Rats were sacrificed under ether anesthesia on the 8th day. The stomach injury was assessed by macroscopic damage and histological study.&#x0D; Results and discussion: The results showed that macroscopic stomach damage scores caused by administration of Indomethacin did not significantly decrease by administration of N-acetylcysteine alone (p&gt;0.05), but it decreased significantly by administration of Amlodipine alone or by its combination with N-acetylcysteine (p&lt;0.05). Microscopic stomach damage scores did not significantly decrease by administration of Amlodipine or N-acetylcysteine alone (p&gt;0.05), but they decreased significantly by administering the combination of Amlodipine with N-acetylcysteine (p&lt;0.05). Administration of Amlodipine with N-acetylcysteine showed significant reduction in the severity of the gastric inflammation induced by Indomethacin, which was evidenced macroscopically and microscopically.&#x0D; Conclusion: This study concluded that administration of Amlodipine with N-acetylcysteine produce obvious enhancement in gastritis induced by Indomethacin.

Comparative pharmacokinetics of four major flavonoids in normal and chronic gastritis rats after oral administration of different combinations of Banxia Xiexin decoction.

Chronic gastritis (CG) has become a major threat to human health. Banxia Xiexin Decoction (BXXXD) has been used clinically to treat gastritis by acting on the spleen and stomach for thousands of years. Baicalin, wogonoside, liquiritin and liquiritigenin are the main bioactive flavonoids of BXXXD. A rapid, sensitive and selective HPLC-triple quadrupole (TQ)-MS/MS method was developed to simultaneously quantify the four flavonoids in rat plasma in this study. With salidroside as internal standard (IS), plasma samples were extracted and separated on a Welch HPLC XB-C18 column (2.1 × 50 mm, 1.8μm) using gradient elution. The optimized gradient of the mobile phase consisted of water (containing 0.1% formic acid) (A) and methanol (B) was used. Detection was implemented in multiple reaction monitoring mode with an electrospray negative ionization source. The comparative pharmacokinetics of four analytes in normal and CG rats after oral administration of BXXXD or its different compatibilities were first investigated. The results indicated that the pharmacokinetic behaviors of analytes were obviously changed in CG rats. From the comparison between the whole prescription group and the compatibility groups, it was found that the pharmacokinetic behavior of analytes also changed to some extent. The pharmacokinetic alterations of analytes might be due to the pathological conditions of CG.

Regulation of gut microbiota of Astragali Radix in treating for chronic atrophic gastritis rats based on metabolomics coupled with 16S rRNA gene sequencing

Astragali Radix (HQ), a common traditional Chinese medicine (TCM), is widely used to treat chronic atrophic gastritis (CAG). However, its mechanism in treating CAG is still not clear. Accumulating evidence highlights the link between gut microbiota and CAG. We hypothesized that the gut microbiota might be involved in the effect of HQ. Ultra-performance liquid chromatography coupled with time-of-flight mass spectrometry (UPLC-Q-TOF/MS) based metabolomics and 16S rRNA gene sequencing techniques of the cecal contents were applied to study its mechanisms. As a result, nine metabolites and fifteen gut microbiotas changed significantly in cecal contents samples between control group and model group. Among them, two metabolites (7-keto-3A ·12-α-hydroxyalkanoic acid and deoxycholic acid) and two gut microbiota genera (Acetobacter and Escherichia), had the most obvious callback effect after the administration of HQ. Sixty-seven correlated pairs exhibited the significant link between the involved metabolites and gut microbiotas through the correlation analysis, where two strong correlation pairs: Tetrahydrohydroxone ∼ Bacteroides (r = 0.895) and Deoxycholic acid ∼ Acetobacter (r = −0.843) were regulated by HQ. The results showed that HQ had the potential protection from metabolic perturbation involved into gut microbiotas induced by CAG. Two gut microbiotas, Acetobacter and Escherichia, and two metabolites, 7-keto-3A ·12-α-hydroxyalkanoic acid and deoxycholic acid were the potential targets of HQ.

Exploration of Tuina Effect and Mechanism in Chronic Atrophic Gastritis Rats.

Chronic atrophic gastritis is a very common condition in the general clinical practice of gastroenterology. Tuina treatment is widely used clinically. The aim of our study was to investigate the mechanisms of tuina in rats with chronic atrophic gastritis. Fifty-six specific pathogen-free grade rats were employed for our study. They were divided into 5 groups and treated differ- ently. Body weight was recorded every week, and their small intestine propulsive ratio was measured after intragastric administration of carbon powder. Histopathological observation of gastric tissues was performed using hematoxylin and eosin staining. The levels of motilin and gastrin in serum were detected by enzyme-linked immunosorbent assay, and the expression levels of Bcl-2 and cytochrome C were measured by the western blot assay. There was no significant difference in body weight and small intestine propulsive ratio between the chronic atrophic gastritis model group and the tuina group (P > .05). However, we can see some significant changes in histomorphology after treatment with tuina. For example, the atrophy of gastric mucosal epithelium and glands had improved, and the inflammatory cells infiltrating the lamina propria were decreased significantly. Moreover, the level of gastrointestinal hormone GAS was increased (P < .001), and there was no statistically significant difference in motilin, Bcl-2, and cytochrome-c after treatment with tuina (P > .05). Our research demonstrated the effectiveness of tuina treatment on chronic atrophic gastritis with a possible underlying mechanism that affected the secretion of gastric acid, which could provide some useful information for clinical application.

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

Ethnopharmacological relevanceGastritis can lead to ulcers and the development of gastric cancer. The rhizome of Atractylodes macrocephala Koidz. (Asteraceae), a traditional Chinese medicinal herb, is prescribed for the treatment of gastric disorders, hepatitis and rheumatism. Its bio-active compounds are considered to be particularly effective in this regard. However, the molecular processes of the herb's anti-inflammatory activity remain obscure. This study elucidates a mechanism upon which an ethanolic extract of this herb (Am-EE) exerts anti-inflammation effects in RAW264.7 macrophage cells (RAW cells) stimulated by lipopolysaccharide (LPS) treatment and HCl Ethanol-stimulated gastritis rats. Aim of the studyTo investigate the anti-gastritis activities of Am-EE and explore the mode of action. Materials and methodsEthanol (95%) was used to prepare Am-EE. The quality of the extract was monitored by HPLC analysis. The in vivo effects of this extract were examined in an HCl Ethanol-stimulated gastritis rat model, while LPS-stimulated RAW cells were used for in vitro assays. Cell viability and nitric oxide (NO) production were observed by MTT and Griess assays. Real-time PCR was used to examine mRNA expression. The PGE2 ELISA kit was employed to detect prostaglandin E2 (PGE2). Enzyme activities and protein contents were examined by immunoblotting. Luciferase reporter gene assays (LRA) were employed to observe nuclear transcription factor (NF)-κB activity. The SPSS (SPSS Inc., Chicago, Illinois, United States) application was used for statistical examination. ResultsHPLC analysis indicates that Am-EE contains atractylenolide-1 (AT-1, 1.33%, w/w) and atractylenolide-2 (AT-2, 1.25%, w/w) (Additional Figure. A1). Gastric tissue damage (induced by HCl Ethanol) was significantly decreased in SD rats following intra-gastric application of 35 mg/kg Am-EE. Indistinguishable to the anti-inflammation effects of 35 mg/kg ranitidine (gastric medication). Am-EE treatment also reduced LPS-mediated nitric oxide (NO) and prostaglandin E2 (PGE2) production. The mRNA and protein synthesis of inducible cyclooxygenase (COX)-2 and NO synthase (iNOS) was down-regulated following treatment in RAW cells. Am-EE decreased NF-κB (p50) nuclear protein levels and inhibited NF-κB-stimulated LRA activity in RAW cells. Lastly, Am-EE decreased the up-regulated levels of phosphorylated IκBα and Akt proteins in rat stomach lysates and in LPS challenged RAW cell samples. ConclusionOur study illustrates that Am-EE suppresses the Akt/IκBα/NF-κB pathway and exerts an anti-inflammatory effect. These novel conclusions provide a pharmacological basis for the clinical use of the A. macrocephala rhizome in the treatment and prevention of gastritis and gastric cancer.