Ethanol-induced Gastric Ulcer In Rats Research Articles

Anti-oxidative stress and gastroprotective effect of Tri-Tharn-Thip tea against ethanol-induced gastric ulcer in rats

BackgroundTri-Tharn-Thip, a traditional Thai medicine, is a herbal formula used to promote milk production, wound healing, and gastric ulcer. However, no previous studies have reported its anti-gastric ulcer activity. This study aimed to evaluate the gastroprotective effects of Tri-Tharn-Thip tea (Tri-TTa) and explore its potential mechanisms of action by measuring the levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), mucin, and inducible nitric oxide synthase (iNOS). MethodsFor this purpose, 24 Wistars rats were divided into four groups. Group I, sham group, received distilled water; Group II, vehicle control group, received distilled water; Group III, positive control group, received omeprazole (20 mg/kg/d); and Group IV, Tri-TTa group, received Tri-TTa (500 mg/kg/d). The treatment protocol lasted 7 d, and all groups except for the sham group received 80 % ethanol on the last day, 4 h before scarification. The gastric tissue was removed; the ulcer area, ulcer score, and pH values were evaluated; and a histopathological examination of the gastric tissue was conducted. ROS, MDA, iNOS, SOD, CAT, and GSH levels were determined using ELISA. ResultsPretreatment with 500 mg/kg Tri-TTa significantly reduced the gastric ulcer area and ROS, MDA, and iNOS levels in rats with ethanol-induced gastric ulcers. Tri-TTa increased the levels of SOD, CAT, and GSH in gastric tissues. Tri-TTa administration also significantly increased mucin content. ConclusionTri-TTa exhibited gastroprotective properties that could be linked to decreased oxidative stress markers and elevated antioxidant enzyme levels.

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

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

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

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

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

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

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

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

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

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

Antiulcerogenic and antioxidant activities of Plantago ovata ethanolic extract in rats.

This study aimed to determine the antiulcerogenic and antioxidant activities of Psyllium (Plantago ovata Forssk) seed ethanolic extract in rats. We assessed the antioxidant potential using free radical scavenging on DPPH, β-carotene bleaching activity, ferric reducing power, and hydroxyl radical scavenging activity. In the antiulcerogenic study, pre-treatment with Plantago ovata seeds ethanolic extract (POE) (400 mg/kg b.wt) significantly protected against ethanol-induced gastric ulcer in rats by decreasing the ulcer index value and preserving the integrity of the gastric mucosa. The oxidative stress status in the stomach tissues showed a significant increase in the antioxidant enzyme levels of superoxide dismutase, catalase, and glutathione peroxidase with a significant decrease in lipid peroxidation during pre-treatment with POE. In conclusion, the POE protects against gastric ulcer due to its antioxidant potential and presence of bioactive molecules.

Protective effect of barbigerone against ethanol-induced ulcers via the interleukins/ICAM-1/Bcl-2 pathway.

The objective of the study was to assess the protective effects of barbigerone in ethanol-induced gastric ulcers in rats. Male Wistar rats (180±20 g) were used in the study (n=06). The rats were randomly divided into different groups, i.e., the normal group, ethanol control, and barbigerone 10 and 20 mg/kg group. Various biochemical parameters were assessed - total acidity and pH values, oxidative stress biomarkers such as superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), and catalase (CAT) along with markers, i.e., tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β, intercellular adhesion molecule-1 (ICAM-1) and expression of B-Cell Leukemia/Lymphoma 2 (Bcl-2). Also, histopathology was performed. Treatment with barbigerone in the ethanol-induced-ulcer rats restored the levels of biochemical parameters such as SOD, GSH, MDA, CAT, and markers expression, including TNF-α, IL-6, IL-1β, ICAM-1, and Bcl-2 with protected against cellular necrosis. Barbigerone protective effects can be attributed to its ability to reduce oxidative stress and inflammation, as well as promote gastroprotection against ethanol-induced ulcers in rats.

Anti-ulcerogenic activity of the powder fraction of leaves of Aspillia africana against ethanol-induced gastric ulcer in rats: Possible role of mucus and antioxidant effect

Massive alcohol drinking can lead to gastric ulcer. In the present study we investigated the gastroprotective effect of powder fraction of the leaves of Apillia africana (AA) in ethanol (EtOH) induced oxidative stress and peptic ulcer in rats. The rats were divided into six treatment groups, which were the normal control group, negative control group (ethanol-induced) and tree treatment groups: AA at the doses of 100 mg/kg body weight (BW), 200 mg/kg BW and 400 mg/kg BW, and the positive control group treated with famotidin at the dose of 100 mg/kg BW. Gastroprotective effect was measured by the ulcerative lesion index, ulcer surface area, percentage of lesion area. Antioxidant and histopathological analyses were also conducted to gain additional data regarding the gastroprotective effect of AA in the rats’ stomachs. AA showed protected the gastric mucosa from ethanol ulceration, as revealed by the improved macroscopic and histological appearance. AA significantly increased the gastric homogenate content of GSH and inhibited the lipid peroxidation as revealed by the reduced gastric content of malondialdehyde (MDA). AA possesses gastro-protective activity, which could be attributed to a mucus production, antioxidant, and regeneration activities.

Retraction: In Vivo Antioxidant and Antiulcer Activity of Parkia speciosa Ethanolic Leaf Extract against Ethanol-Induced Gastric Ulcer in Rats.

Retraction: In Vivo Antioxidant and Antiulcer Activity of Parkia speciosa Ethanolic Leaf Extract against Ethanol-Induced Gastric Ulcer in Rats.

Mechanisms of anti-ulcer actions of Prangos pabularia (L.) in ethanol-induced gastric ulcer in rats

Peptic ulcer disease is the greatest digestive disorder that has increased incidence and recurrence rates across all nations. Prangos pabularia (L.) has been well documented as a folkloric medicinal herb utilized for multiple disease conditions including gastric ulcers. Hence, the target study was investigation the gastro-protection effects of root extracts of Prangos pabularia (REPP) on ethanol-mediated stomach injury in rats. Sprague Dawley rats were clustered in 5 cages: A and B, normal and ulcer control rats pre-ingested with 1 % carboxymethyl cellulose (CMC)); C, reference rats had 20 mg/kg omeprazole; D and E, rats pre-supplemented with 250 and 500 mg/kg of REPP, respectively. After one hour, group A was given orally 1 % CMC, and groups B-E were given 100 % ethanol. The ulcer area, gastric acidity, and gastric wall mucus of all stomachs were determined. The gastric tissue homogenates were examined for antioxidant and MDA contents. Moreover, the gastric tissues were analyzed by histopathological and immunohistochemically assays. Acute toxicity results showed lack of any toxic effects or histological changes in rats exposed to 2 and 5 g/kg of REPP ingestion. The ulcer controls had extensive gastric mucosal damage with lower gastric juice and a reduced gastric pH. REPP treatment caused a significant reduction of the ethanol-induced gastric lacerations represented by an upsurge in gastric mucus and gastric wall glycoproteins (increased PAS), a decrease in the gastric acidity, leukocyte infiltration, positively modulated Bax and HSP 70 proteins, consequently lowered ulcer areas. REPP supplementation positively modulated oxidative stress (increased SOD, CAT, PGE2, and reduced MDA) and inflammatory cytokines (decreased serum TNF-α, IL-6, and increased IL-10) levels. The outcomes could be scientific evidence to back-up the folkloric use of A. Judaica as a medicinal remedy for oxidative stress-related disorders (gastric ulcer).

Characterization and gastroprotective effects of Rosa brunonii Lindl. fruit on gastric mucosal injury in experimental rats - A preliminary study.

Gastric ulcer is the most prevalent disorder affecting a large population. Rosa brunonii Lindl. fruit (RBF) has traditionally been used to treat stomach pains. Therefore, the current work aimed to isolate, characterize, and investigate the gastro-protective effect of Rosa brunonii Lindl. fruit chloroform extract (RBFCE) against ethanol-induced gastric ulcers in rats. Quercetin 3-O-glucoside (QUE-G) was isolated and characterized by modern spectroscopic techniques. RBFCE was orally administered at 250 mg/kg, 500 mg/kg, and 750 mg/kg doses for ten days. Gastric ulcer was induced by a single dose of absolute ethanol (5 ml/kg) on the last day of the study. Histological changes were calculated, along with ulcer inhibition and the ulcer index (UI). Gastric juice volume, pH, acidity, mucus content, and protein content were evaluated to understand the mechanism underlying its gastroprotective effect. Omeprazole (OMP) was used as the positive control. RBFCE at a dose of 750 mg/kg significantly (p<0.01) reduced the UI (3.54) and increased the protection rate (67.63%) compared to the negative (ulcer) control group. Treatment with RBFCE in a dose-dependent manner increased the gastric pH, mucus content, and total protein while decreasing gastric juice volume and total acidity. Histopathological studies showed severe gastric mucosal injury and edema in ulcer control animals compared to extract-treated groups. This study demonstrated that oral administration of RBFCE possesses a significant gastroprotective effect due to its anti-secretory and cytoprotective mechanisms. Our findings support the traditional use of RBF to treat the gastric ulcer.

Silver nanoparticles synthesized from Quercus brantii ameliorated ethanol-induced gastric ulcers in rats by decreasing oxidative stress and improving antioxidant systems.

Gastric ulcers are caused by an imbalance between aggressive and defensive factors. The green synthesis of silver nanoparticles is becoming a new and promising method in the treatment of gastrointestinal ulcers. This study was conducted to investigate the protective and antioxidant effects of silver nanoparticles synthesized from Quercus brantii extract (NSQBE) on gastric damage induced by alcohol in rats. In this study, silver nanoparticles were produced by the green synthesis method using oak extract. The structure and morphology of nanoparticles were confirmed by various techniques such as UV-Vis spectroscopy, fourier transforms infrared spectrometer (FTIR), scanning electron microscope (SEM), transmission electron microscopy (TEM), X-ray diffraction (XRD), energy-dispersive X-rayanalysis(EDX), and dynamic light scattering )DLS(. For the animal studies, 30 male Wistar rats weighing 200 ± 20g were randomly selected and divided into five groups (the normal, ethanolic, NSQBE treatment (received doses of 20 and 5mg/kg), and standard (received a dose of 50mg/kg of ranitidine) groups. After the rats were euthanized, their stomach was removed. A part of the stomach tissue of rats was used for histopathological studies, and the other part was used to study biochemical parameters such as the level of reactive oxygen species (ROS), protein carbonyl oxidation (PCO), malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH) as well as nitric oxide (NO). Our results showed that in the ethanol group, the levels of ROS, MDA, PCO, and serum NO were higher than in the normal group. In addition, reduced GSH, CAT, SOD, tissue NO, gastric mucus, and antioxidant potential were decreased. In rats pretreated with NSQBE and ranitidine, the levels of ROS, MDA, PCO, and serum NO decreased, and the levels of GSH, CAT, SOD, tissue NO, gastric mucus, and antioxidant potential were increased in comparison to the ethanol group. The results of this study showed that silver nanoparticles synthesized using Quercus brantii are a promising approach for the treatment of gastric ulcers.

Metabolites Profiling and Bioassays Reveal Bassia indica Ethanol Extract Protective Effect against Stomach Ulcers Development via HMGB1/TLR-4/NF-κB Pathway.

Clinical manifestation of gastric ulcers is frequent, in addition to their costly drug regimens, warranting the development of novel drugs at lower costs. Although Bassia indica is well characterized for its anti-inflammatory and antioxidant potential, capacity of its ethanol extract (BIEE) to prevent stomach ulcers' progression has not been reported. A nuclear protein termed high-mobility group box 1 (HMGB1) plays a key role in the formation of stomach ulcers by triggering a number of inflammatory responses. The main purpose of the current investigation was to evaluate the in vivo anti-inflammatory and anti-ulcerogenic capabilities of BIEE against ethanol-induced gastric ulcers in rats via the HMGB1/TLR-4/NF-B signaling pathway. HMGB1 and Nuclear factor kappa (NF-B) expression, IL-1β and Nrf2 contents showed an increase along with ulcer development, concurrent with an increase in immunohistochemical TLR-4 level. In contrast, pre-treatment with BIEE significantly reduced HMGB1 and Nuclear factor kappa (NF-B) expression levels, IL-1β and Nrf2 contents and ulcer index value. Such protective action was further confirmed based on histological and immunohistochemical TLR-4 assays. Untargeted analysis via UPLC-ESI-Qtof-MS has allowed for the comprehensive characterization of 40 metabolites in BIEE mostly belonged to two main chemical classes, viz., flavonoids and lipids. These key metabolites, particularly flavonoids, suggesting a mediation for the anti-inflammatory and anti-ulcerogenic properties of BIEE, pose it as a promising natural drug regimen for treatment of stomach ulcers.

Gastroprotective effects of Polygonatum odoratum in rodents by regulation of apoptotic proteins and inflammatory cytokines

In an increasing interest in natural antiulcer compounds that may have gastric healing effects and possibly prevent ulcer recurrence, Polygonatum odoratum appears as a strong candidate. The gastroprotective potentials of P. odoratum rhizome extract (PORE) were explored on ethanol-induced gastric ulceration in rats. Sprague Dawley rats were caged in 5 groups, normal and ulcer control rats received CMC (1% carboxymethyl cellulose). Omeprazole (20 mg/kg) was given to reference Rats. Experimental rats were treated with 250 mg/kg and 500 mg/kg PORE, respectively. After an hour, the normal control rats received 1% CMC, whereas rat groups 2–5 were given absolute ethanol by oral gavage. After 60 min, rats received anesthesia and were sacrificed. Dissected gastric tissue was analyzed by histopathological and immunohistochemical techniques. PORE treatment significantly lowered the ethanol-induced gastric injury, as shown by up-surging gastric pH and mucus content, reduced leukocyte infiltration, lower ulcerative areas in mucosal layers, and increased antioxidants (SOD and CAT) and (MDA) levels. Furthermore, PORE pre-treated rats showed significantly increased expression of the Periodic acid-Schiff (PAS), HSP-70 protein, and decreased Bax protein in their gastric epithelial layers. PORE treatment showed an important regulation of inflammatory cytokines shown by decreasing the TNF-a, and IL-6 and increasing the IL-10 values. The detected biological activity of PORE is encouraging and presents the scientific evidence for its traditional use as a gastroprotection agent however further studies are required to determine the exact phytochemicals and mechanism pathway responsible for this bioactivity.

GC-MS and Antioxidative Effects of Poly Herbal Formulation of Persea americana Seed Against Ethanol-Induced Gastric Ulcer in Rats

GC-MS and Antioxidative Effects of Poly Herbal Formulation of Persea americana Seed Against Ethanol-Induced Gastric Ulcer in Rats

Gastro-protective Effect of Carica papaya Leaf Extracts on Ethanol-Induced Gastric Ulcer in Rats

Carica papaya leaves are commonly used traditionally to treat many diseases, including peptic ulcers; however, these pharmacological claims and safety issues of the leaves have not been adequately resolved. The present study aims to evaluate the possible gastro-protective potential of Carica papaya aqueous and methanol leaf extracts on ethanol-induced ulcers. Aqueous and Methanol extracts of C. papaya were prepared by percolation method and screened for phytochemicals using conventional method and Gas Chromatography-Mass spectrometric methods. The gastro-protective effects of the extracts were determined using thirty (30) rats weighing 180 and 250 g were randomly divided into five groups. Group 1 served as the normal control (distilled water), groups 2 served as the (negative control), group 3 received 25mg/kg Omeprazole (standard drug) group 4 and 5 received 300 mg/kg and 600 mg/kg of aqueous and methanol extracts of Carica papaya. Two weeks after the oral administration, gastric ulcer was induced in all rats with 95% ethanol (2 mL). The aqueous and methanol leaf extract of C. papaya showed a significant (p&lt;0.05) dose-dependent protection against peptic ulcer. The effects produced by the methanol leaf extract of C. papaya were comparable to those of the standard drugs (Omeprazole). Phytochemical analysis of the aqueous and methanol leaves extracts of C. papaya revealed the presence of flavonoids, tannins, alkaloids, terpenoids, cardiac glycosides, reducing sugar and saponins, some of which have been reported to elicit cytoprotective effect. Gas chromatographic analysis showed the presence of cytoprotective agents. These findings show that aqueous and methanol extracts of the leaves of C. papaya possess potent antiulcer properties; hence justifies the traditional usage of this plant for ulcer treatment.

Bletilla striata Polysaccharide Nanoparticles Improved the Therapeutic Efficacy of Omeprazole on the Rat Gastric Ulcer Induced by Ethanol.

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.

LC-ESI-MS phenolic contents assessment, antioxidant, and protective ability of Punica granatum root bark extract against ethanol-induced gastric ulcer in rats: in silico H+, K+-ATPase inhibitory pathway study.

The objectives of the current study were to evaluate the Punica granatum root bark extract's (PGE) antioxidant and gastroprotective activities against ethanol-induced gastric ulcers in Wistar rats and to elucidate the putative mechanism of action using in silico analysis. The PGE phytochemical study shows high levels of phenolics, flavonoids, tannins, and polysaccharides. In vitro, the PGE was more effective at scavenging hydroxyl radicals than quercetin and had lower ferric reducing activity than catechin. In vivo, it was revealed that pretreatment of ethanol-ulcerated rats with PGE at oral doses of 100, 200, and 400mg/kg b.w. offered a dose-dependent shield against ethanol-induced ulcers when compared to Omeprazole (20mg/kg b.w.) by preventing the development of deep ulcer lesions, lowering gastric juice output and pH rises, boosting gastric mucus production and antioxidant enzyme levels, and attenuating malondialdehyde and myeloperoxidase contents. Moreover, the liquid chromatography-mass spectrometry analysis of PGE identified 5 phenolic acids and 4 flavonoids, which revealed an in silico high oral bioavailability, drug-likenesses, and good binding affinities and thus inhibitory effects on the gastric H+, K+-ATPase enzyme. PGE may have synergistic antioxidant, anti-inflammatory, and H+, K+-proton pump inhibitory actions that contribute to its antiulcer efficacy.

Gastroprotective effects of ginsenoside Rh4 against ethanol-induced gastric mucosal injury by inhibiting the MAPK/NF-κB signaling pathway.

Ginsenoside Rh4, a bioactive component extracted from Panax ginseng, exhibits various pharmacological activities, such as anti-inflammatory, anti-oxidation, anti-diabetes, anti-obesity, antitumor and immunity enhancement. However, the gastroprotective effect of ginsenoside Rh4 remains unknown. The present study evaluated the gastroprotective effect and potential mechanism of ginsenoside Rh4 in an ethanol-induced gastric ulcer model. Ginsenoside Rh4 (15, 30, and 60 mg kg-1) and omeprazole (30 mg kg-1) were administered orally for 7 days. The results showed that pretreatment with ginsenoside Rh4 reduced the gastric injury area and percentage of mucosal lesions in gastric tissue. Besides, treatment with ginsenoside Rh4 increased superoxide dismutase (SOD) activity, glutathione (GSH) and nitric oxide (NO) levels, reduced the content of malonaldehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), mediated the prostaglandin E-2-cyclooxygenase-2 (PGE2-Cox-2) pathway, and mitigated inflammation and oxidative stress via blockade of proinflammatory mitogen-activated protein kinase-nuclear factor κB (MAPK/NF-κB) signaling pathways. Furthermore, ginsenoside Rh4 significantly enhanced the protein expression of B-cell lymphoma gene 2 (Bcl-2), decreased the protein expression of Bcl-2-associated X protein (Bax) and tumor necrosis factor receptor superfamily member 6 (Fas), and inhibited the number of apoptotic cells in gastric tissues. The present work demonstrated that ginsenoside Rh4 exerted a considerable gastroprotective effect against ethanol-induced gastric ulcers in rats.