Ethanol-induced Gastric Mucosal Injury Research Articles

The Gastroprotective Effect of Small Molecule Oligopeptides Isolated from Walnut (Juglans regia L.) against Ethanol-Induced Gastric Mucosal Injury in Rats.

The study investigated the protective effect of walnut oligopeptides (WOPs) against ethanol-induced gastric injury using Sprague-Dawley (SD) rats. Rats were randomly divided into seven groups based on body weight (10/group), normal group, ethanol group, whey protein group (220 mg/kg body weight), omeprazole group (20 mg/kg body weight), and three WOPs groups (220, 440, 880 mg/kg body weight). After 30 days of treatment with WOPs, rats were given 5 mL/kg absolute ethanol by gavage to induce gastric mucosal injury. Gastric ulcer index (GUI) were determined and the following measured; gastric content pH, gastric mucin, endogenous pepsinogens (PG), prostaglandin E2 (PGE2), inflammatory cytokines, oxidative stress indicators, and the expression of apoptosis-related proteins were measured to evaluate the gastroprotective effect of WOPs. The results showed that the administration with WOPs markedly mitigated the hemorrhagic gastric lesions caused by ethanol in rats, and decreased the GUI, the gastric content pH, PG1, PG2, and NO levels, enhanced mucin and PGE2. Also, WOPs repressed gastric inflammation through the reduction of TNF-α, IL-6, IL-1β and increase IL-10 levels, and revealed antioxidant properties with the enhancement of superoxide dismutase, glutathione, and catalase activity, while reduction of malondialdehyde. Moreover, WOPs treatment significantly down-regulated Bax, caspase-3 and nuclear factor-κB p65 (NF-κB p65) expression, while up-regulating the expression of Bcl-2 and inhibitor kappa Bα (IκBα) protein. These results indicated that WOPs have protective effects against ethanol-induced gastric mucosal injury in rats through anti-inflammatory, anti-oxidation, and anti-apoptosis mechanisms.

Novel role of probiotics in improving cell proliferation and regulating proinflammatory cytokine-mediated oxidative damage of ethanol-induced gastric mucosal injury in rats

Gastric ulcer is a common chronic disease in human digestive system. Excessive alcohol drinking can lead to gastric ulcer. The gastroprotective effect and molecular mechanisms of probiotics in a rat model of ethanol-induced gastric injury were evaluated. Thirty five rats divided into five equal groups. Group 1 :( Control normal) rats received no drugs. Group 2 :(Early ulcer) rats received absolute ethanol (0.5ml/100g rat) orally on empty stomach and sacrificed one hour later. Group 3 :( Early ulcer + Probiotics protected) rats received probiotic orally (135 mg/kg b.wt/day) for 3 weeks before ethanol administration then sacrificed after one hour. Group 4: (Late ulcer) rats received ethanol similar to group 2 and sacrificed after 21 days. Group 5: (Late ulcer + Probiotics treated) rats first administered with ethanol and after one hour probiotic was administered for 21 days. A significant increase in L-MDA with marked decrease in GSH and CAT were shown in stomach of gastric injury-induced in rats compared with control group. Conversely, a significant decrease in L-MDA and obvious increase in GSH and CAT were observed after probiotics treatment compared to ulcerated rats. Likewise, a significant up-regulation of NF-κB gene expression level was observed in stomach of gastric injury-induced in rats. This expression was downregulated after probiotics administration. Meanwhile, a significant down-regulation of PPARγ and TGF-β1 gene were detected in gastric injury-induced rats. This expression was upregulated after probiotics administration. Conclusively, probiotics improving gastric cell proliferation and protect gastric mucosa against injury-induced in rats via anti-inflammatory and anti-oxidative mechanisms.

Anti-ulcerogenic activity of Gum Arabic in gastric mucosal injury induced by ethanol in male albino rats

The present study was performed to evaluate the anti-ulcerogenic activity of Acacia senegal (Gum Arabic) against ethanol-induced gastric mucosal injury in rats. Thirty-six adult male albino rats were divided into 4 groups: group 1 served as a control; group 2 consisted of rats that received 15% of gum in drinking water for 2 weeks; group 3 comprised ulcerated animals administered 5 mL of ethanol/kg body weight by gavage; and group 4 consisted of rats received 15% of gum in drinking water for 2 weeks before ethanol administration. Superoxide dismutase (SOD) glutathione peroxidase (GPx), malondialdehyde (MDA), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), interleukin (IL)-B1), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total protein, and albumin were assayed in addition to histological study. The results revealed that ethanol decreased SOD, GPx, and PGE2 in tissue and serum total protein and albumin, while increased MDA in tissue, serum TNF-α, IL-B1, PGE2, ALT, AST, and ALP. Histological findings showed less edema and leucocytes infiltration compared with ulcer group. Furthermore, gum administration elevated PGE2, SOD, and GPx and significantly reduced MDA, TNF-α, and IL-B2. In conclusion, Gum Arabic can enhance gastric protection and sustain the integrity of the gastric mucosa. Novelty The selected dose of Gum Arabic has the ability to decrease the pro-inflammatory cytokines in plasma and gastric tissue, thus enhancing gastric protection and maintaining the integrity of the gastric mucosa. Gum Arabic can compensate for the loss of antioxidants.

Protective effects of genipin on ethanol-induced acute gastric injury in mice by inhibiting NLRP3 inflammasome activation

Genipin has been shown to exert anti-inflammatory effects, but its mechanism in protecting the ethanol-induced acute gastric injuries remains largely unclear. The present study aimed to investigate the effects of genipin on ethanol-induced acute gastric injuries in mice. After intragastrical administration of genipin for 7 consecutive days, acute gastric injuries were induced in the mice by ethanol treatment for 1 h. The expression levels of MDA, MPO, SOD, CAT, and NO in gastric tissues, and the levels of IL-6, TNF-α, MTL, SP, VIP and SS in serum samples were measured by ELISA. In addition, Western blotting was used to determine the expression levels of proteins involved in NLRP3 signaling pathway. The findings revealed that oral administration of genipin significantly ameliorated the pathological injury of gastric mucosa induced by ethanol, decreased the oxidative stress induced by ethanol and suppressed the expression levels of in-flammatory cytokines in gastric tissues and serum samples. In addition, it was observed that oral administration of genipin could remarkably inhibit the expression levels of related proteins in the NLRP3 signaling pathway. In conclusion, these results suggest that genipin may exhibit protective roles in ethanol-induced gastric mucosal injuries by activating antioxidant system and attenuating inflammatory reaction.

Astragaloside IV Protects Ethanol-Induced Gastric Mucosal Injury by Preventing Mitochondrial Oxidative Stress and the Activation of Mitochondrial Pathway Apoptosis in Rats.

Alcohol consumption affects gastric mucosa by multiple and complex mechanisms depending either by direct contact of ethanol or by indirect biological damage induced by its metabolite acetaldehyde. The present study aims at further investigating the mechanism of ethanol-induced gastric mucosa injury and the protective effect of astragaloside IV (AS-IV) in an aspect of mitochondrial oxidative stress and mitochondrial pathway of apoptosis. Using an array of experimental approaches, we have shown that the development of mitochondrial oxidative stress and associated apoptosis play crucial roles in the pathogenesis of gastric injury induced by ethanol. AS-IV inhibits mitochondrial oxidative stress by scavenging accumulation of malondialdehyde and decreasing the consumption of glutathione. AS-IV also prevents ethanol-induced apoptosis by modulating the activity of caspase-3 and caspase-9, the expression of Bax/Bcl-2, and the release of cytochrome C and apoptosis inducing factor. Moreover, AS-IV reduces ethanol-mediated activation of caspase-8 and breakage of Bid. This study thus indicates that AS-IV prevented ethanol-induced gastric damage by blocking activation of mitochondrial oxidative stress and mitochondrial pathway of apoptosis induced by ethanol in the gastric mucosa.

Targeting MAPKs, NF-κB, and PI3K/AKT pathways by methyl palmitate ameliorates ethanol-induced gastric mucosal injury in rats.

Excessive drinking of alcohol has been frequently associated with gastric injury; however, its underlying molecular mechanisms have been inadequately investigated. Methyl palmitate (MP) has demonstrated marked hepato-, cardio- and pulmonary protective features; however, its effects on ethanol-induced gastric injury have not been studied. The aim of the present study was to evaluate the potential gastroprotective activity of MP against ethanol-evoked gastric mucosal damage in rats and associated molecular mechanisms, for example, mitogen-activated protein kinases (MAPKs), nuclear factor κB (NF-κB), and phosphoinositide 3 kinase/protein kinase B (PI3K/AKT) pathways. The rat stomachs were examined in terms of the inflammatory, oxidative, and apoptotic perturbations. Current data demonstrated that pretreatment with MP attenuated the gross gastric damage, scores of ulcer index, area of mucosal lesions and histopathology outcomes; actions which were similar to the reference antiulcer omeprazole. MP inhibited NF-κB expression, its nuclear translocation, and the expression of its downstream signals, for example, tumor necrosis factor-α and myeloperoxidase besides restoration of interleukin-10 levels. Western blot analysis revealed that MP counteracted the disruption of MAPKs signaling via lowering p-c-Jun N-terminal kinase 1/2 (p-JNK1/2) expression and restoring the phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2) levels without affecting p-p38MAPK levels. Additionally, MP improved the antioxidant milieu via diminishing lipid peroxides and enhancing glutathione, glutathione peroxidase, total antioxidant capacity and mucosal nitric oxide. In the context of apoptosis, MP inhibited the cleavage of caspase-3 and poly(ADP-ribose)polymerase (PARP) and Bax protein expression with upregulating B cell lymphoma-2 expression (Bcl-2), thus, promoting gastric cellular survival. This was confirmed by MP activation of the PI3K/AKT pathway manifested by enhanced expression of PI3K p110α and p-AKT. Together, the present findings report the gastroprotective actions of MP mediated via its anti-inflammatory, antioxidant, and antiapoptotic actions. The underlying molecular mechanisms involve, at least partly, the modulation of MAPKs, NF-κB and PI3K/AKT transduction.

Antiulcerogenic Activity of methanol extract and solvent fractions of Stem Bark of Lannea acida (A. Rich) Against Ethanol-Induced Gastric Mucosal Injury in Albino Rats

Peptic ulcer disease is one of the most prevalent gastrointestinal disorders causing tremendous human suffering worldwide. The present study was designed to evaluate the antiulcerogenic activity of the methanol and solvent stem bark fractions (hexane, ethyl acetate and butanol) and elucidate their possible antiulcerogenic mechanisms. The antiulcerogenic mechanisms were investigated by estimation of Superoxide dismutase (SOD), Glutathione (GSH), Catalase (CAT), Vitamins A, C and E, Malondialdehyde (MDA) and involvement of KATp channel. Pretreatment with the methanol extract and solvent fractions produce significant reductions in ulcer index in a dose dependent manner. Ethylacetate fraction (EtyAc) showed the highest antiulcer activity. Elevated MDA and decreased levels of SOD, GSH, CAT, Vitamin A, C and E observed in ulcer control groups were significantly decreased and increased respectively in the EtyAc fraction treated groups. Antiulcer activity of the EtyAc fraction was blocked upon coadministration with glibenclamide; a KATp channel blocker. The stem bark extract of Lannea acida possess antiulcerogenic activity and the mechanisms seems to involve antioxidant activity and KATp channel opening.

Corrigendum to "Acute Toxicity and Gastroprotective Role of M. pruriens in Ethanol-Induced Gastric Mucosal Injuries in Rats".

[This corrects the article DOI: 10.1155/2013/974185.].

Gastroprotective effect of apricot kernel oil in ethanol-induced gastric mucosal injury in rats

ABSTRACT We investigated the gastroprotective effect of apricot kernel oil on ethanol induced gastric ulcer in rats. Male Wistar albino rats were divided into control, ethanol and apricot kernel oil + ethanol groups. The fatty acid composition of apricot kernel oil was determined using GC-MS. A gastric ulcer index was defined as the area percentage of the gastric mucosa consisting of ulcerated tissue. Gastric tissue was investigated by TUNEL staining for apoptosis, immunohistochemical iNOS staining, measurement of gastric IL-10 and IL-6 expression by ELISA and assays of catalase, malondialdehyde and superoxide dismutase. The ethanol group exhibited a higher gastric ulcer score, increased IL-6 level, increased number of inducible nitric oxide synthase-positive and TUNEL positive cells, and a higher MDA level compared to the control group. The apricot kernel oil + ethanol group exhibited significantly fewer gastric lesions compared to the ethanol group. Apricot kernel oil protects rat gastric mucosa against ethanol induced injury by its anti-inflammatory, anti-oxidative and anti-apoptotic effects, and might be useful for reducing the severity of gastric ulcers.

English

Indomethacin is commonly used as an anti-inflammatory and pain relieving medication; however, it has the side effect of gastric ulcer formation which is an actual common gastrointestinal illness that may result in dangerous complications and even death. Various diseases have been treated widely by the use of oriental herbal medicines, this study aims to evaluate the antiulcerative and antioxidative effect of two doses (100 and 50 of Moringa oleifera ethanolic leaf extract; MOELE) on indomethacin plus ethanol-induced oxidative gastric mucosal injury in rats. Sixty adult males Wistar rats weighing 170 to 200 g, were divided into equal six groups. First group of rats were administered saline as a vehicle, second group of rats were given indomethacin (15 mg/kg), third and fourth groups of rats were giving MOELE 100 and 500 mg, fifth group of rats were given indomethacin+ MOELE 100 mg, and sixth group of rats were administered with indomethacin + MOELE (500 mg). To study the effect of MOELE on oxidative gastric mucosal injury in rats, two doses were administered 2 h before ulcer induction by indomethacin plus ethanol. The administration continued for two weeks. All rats were sacrificed 24 h after the last dose. Indomethacin group showed significant increases in lesion index (LI) and increase in malondialdehyde (MDA) level, while there was a decrease in superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) activities when compared with the control group (G1). MOELE with two doses mentioned before (groups 5 and 6) were effective to reduce stomach LI and oxidative stress markers (MDA) while increasing significantly the antioxidant biomarkers (SOD, GST, and GPx) compared with indomethacin group (G2). A highly significant decrease in MDA accompanied by a marked increase in SOD, GST, and GPx were recorded in group 6. The results concluded that MOELE has an effective antiulcer and antioxidant activities. It can scavenge the free radicals and protect gastric against ulceration. Also, MOELE could ameliorate the ulcerative side effect of indomethacin. Key words: Moringa oleifera, antioxidant enzymes, indomethacin, lesion index, lipid peroxidation.

In vivo anti-ulcerogenic effect of okra (Abelmoschus esculentus) on ethanol-induced acute gastric mucosal lesions

Context: Okra, Abelmoschus esculentus (L.) (Malvaceae), is a medicinal plant widely used in Turkish traditional medicine for the treatment of various diseases such as ulcers and gastritis.Objective: In the present study, we evaluated the gastroprotective effect of okra against ethanol-induced acute gastric mucosal injury in animal models.Materials and methods: Wistar rats were treated with 500, 250 or 100 mg/kg okra; 20 mg/kg famotidine (Fam); and 75 mg/kg quercetin (Que). Following a 60 min period, all the rats were given 1 mL of ethanol (80%). One hour after the administration of ethanol, all groups were sacrificed.Results: At 5000 mg/kg, the extract produced (okra) no signs of toxicity in animals. Okra 500, 250, 100, Fam 20 and Que 75 inhibited ulcer formation by 81.0, 67.5, 67.0, 76.3 and 72.4%, respectively. Okra 500 significantly decreased edema, hemorrhage and inflammation scores compared with the ethanol group (p < 0.05). The oxidant levels decreased significantly in the all study groups compared within ethanol group (p < 0.001). Serum β-carotene and retinol levels significantly increased 40.2 and 45.4% in the okra 500 group. In okra 500, 250 and Fam 20 groups, apoptosis significantly decreased (p < 0.001), while okra 500, 250 and Fam 20 groups showed a higher percentage of cell proliferation compared with the ethanol group (p < 0.001).Discussion and conclusions: Our in vivo data indicate that okra has a gastroprotective effect against ethanol and could reduce the gastric ulcer as seen from biochemical and histopathological results. We suggest that okra could be a possible therapeutic antiulcer agent.

Protective effect of gentiopicroside from Gentiana macrophylla Pall. in ethanol-induced gastric mucosal injury in mice.

Gentiopicroside isolated from gentiana macrophylla Pall. belongs to iridoid glycosides. This study aimed to evaluate the protective effect of gentiopicroside against ethanol-induced gastric mucosal injury in mice. Mice were proactively administrated with gentiopicroside by intragastric administration once a day for 3 consecutive days. On the 3rd day, gastric ulcer in mice was induced with 70% ethanol after the last intragastric administration. The stomach tissues were submitted for evaluation of the severity of gastric mucosal alterations. Gentiopicroside administrated orally ameliorated the severity of gastric mucosal alterations. Oral administration of gentiopicroside significantly increased heat shock protein-70 and glutathione levels and superoxide dismutase activity, normalized epidermal growth factor and vascular endothelial growth factor levels, and decreased the levels of tumour necrosis factor-α, interleukin-6 and malondialdehyde, and myeloperoxidase activity in gastric tissue. These findings demonstrated that gentiopicroside has protective effect against ethanol-induced gastric mucosal injury in mice through the improvements of antioxidative and anti-inflammatory effects, as well as up-regulation of heat shock protein-70 level and normalization of epidermal growth factor and vascular endothelial growth factor levels. The results presented in this study provide some evidence for the development of a novel antigastric ulcer agent.

Gastroprotective effect of mature silkworm, Bombyx mori against ethanol-induced gastric mucosal injuries in rats

Gastric ulcer is a clinical condition characterized by ulceration of the surface of the gastric mucosa. Alcohol consumption has been identified as a major cause of gastric ulceration. The silkworm, Bombyx mori, produces diverse functional materials including silk proteins. Here, we evaluated whether Steamed and freeze-dried Mature Silkworm larval Powder (SMSP) can prevent ethanol-induced gastric injury in rats. Sprague-Dawley rats pretreated with SMSP (0.1 or 1 g/kg body weight) or normal diet (AIN-76A) were subjected to intragastric administration of absolute ethanol (3 g/kg body weight, 3 h). Pretreatment with SMSP significantly prevented ethanol-induced gastric mucosal ulceration and hemorrhagic injury, by which improved the total antioxidant capacity and mucus secretion and suppressed the pro-inflammatory responses through inhibiting the recruitment of immune cells. SMSP exerted protective effects in ethanol-induced gastritis via the regulation of anti-oxidative and pro-inflammatory signaling pathway, suggesting SMSP could be anticipating remedy for the treatment of ethanol-induced gastric injury.

The effect of Astragaloside IV on ethanol-induced gastric mucosal injury in rats: Involvement of inflammation

The present study aimed to investigate the potential protective effects of Astragaloside IV (AS-IV) against ethanol-induced gastric mucosal injury in rats. The animals were divided into 7 groups and pretreated with vehicle, various doses of AS-IV (1,2 and 4mg/kg, i.p.) or omeprazole (40mg/kg), 75min later, the gastric mucosal injury was induced by oral administration of ethanol. One hour after ethanol ingestion, the rats were euthanized and gastric tissues were collected to biochemical analyze. Myeloperoxidase (MPO), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), interleukin 10 (IL-10), nuclear factor kappa B (NF-κB) p65 protein, TNF receptor-associated factor 2 (TRAF2) and nuclear NF-κB (nNF-κB) proteins were estimated by enzyme-linked immunosorbent assay or western blot analysis. The gastric mucosal lesions were assessed by macroscopic and histopathological examinations. The results showed pretreatment with AS-IV attenuated the severity of ethanol gastric mucosal damage as evidenced by lowering of injury scores, histopathologic aberrations and leukocyte invasion. These actions were analogous to the reference omeprazole. AS-IV suppressed gastric inflammation by curbing of MPO, TNF-α levels along with NF-κB p65 and TRAF2 expression. It also augmented the anti-inflammatory IL-10 levels. Meanwhile, AS-IV could inhibit NF-κB transcription by inhibiting the expression of NF-κB p65 and increasing the expression of nNF-κB. It seems that AS-IV as an anti-inflammatory agent may have a protective effect against ethanol-induced mucosal injury by inhibition of neutrophil infiltration and reducing the expression of NF-κB p65, TRAF2 and inflammatory cytokines via regulating TNF-α/NF-κB signal pathway in gastric tissue.

Gastroprotective effect of aucubin against ethanol-induced gastric mucosal injury in mice

AimsAucubin, an iridoid glycoside, was isolated from seeds of Eucommia ulmoides Oliver. This study was aimed to evaluate the protective effect of aucubin against ethanol-induced gastric mucosal injury in mice. Materials and methodsMice were orally administrated with aucubin (20, 40 and 80mg/kg) for 3 consecutive days. On the 3rd day, the mice of gastric mucosal injury were induced with 70% ethanol after the last administration of aucubin. Gastric tissue of mice were submitted for evaluating the severity of gastric mucosal injury. The protective effect of aucubin was evaluated by the gastric ulcer index and histological examinations and determining the levels of inflammatory cytokines, oxidative stress and some gastric mucosal protection factors. Key findingsProphylactic oral administration of aucubin decreased gastric ulcer indexes and histological scores. A significant decrease of myeloperoxidase (MPO) activity and the levels of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were observed in aucubin administrated groups. In addition, mice administrated with aucubin increased glutathione (GSH) and heat shock protein-70 (HSP-70) levels and superoxide dismutase (SOD) activity, as well as normalized the levels of epidermal growth factor (EGF), vascular endothelial growth factor (VEGF) and cyclooxygenase-1 (COX-1) in gastric tissue of mice. SignificanceThe findings of this study demonstrated that aucubin shows protective effect against ethanol-induced acute gastric mucosal injury through its anti-inflammatory and anti-oxidant effects. Furthermore, aucubin enhanced gastric mucosal protection by up-regulation of HSP-70 level and normalization of EGF, VEGF and COX-1 levels.

The anti-gastric ulcer effects of combined administration of Bletilla striata and Radix aconiti preparata in mice on the basis of uniform design

Objective To study the influence of the combined administration of Bletilla striata and Radix aconiti preparata with different doses or ratios on anhydrous ethanol-induced gastric mucosal injury in mice with gastric ulcer. Methods The uniform design method was adopted on the basis of two factors and seven levels, which aims to investigate the influence of combined oral administration of Bletilla striata and Radix aconiti preparata with different doses or ratios on gastric mucosal injury in the mice with gastric ulcer. The indices like gastric ulcer index and stomach mucosa damage index were used to help selecting the right dose or ratio of decoctions for further study. Results The combined administration of Bletilla striata and Radix aconiti preparata at a certain proportion could reduce gastric ulcer index and stomach mucosa damage index. According to the regression analysis, the gastric ulcer index and stomach mucosa damage index were obviously inhibited by Bletilla striata, while this function decreased with the combined administration of Bletilla striata and Radix aconiti preparata. However, an interactive effect between each other has not been found. The influence of decoctions on the gastric ulcer index and stomach mucosa damage index became less when the compatibility ratio of Radix aconiti preparata increased, which referred to the total dose ranged between 3.64 g/kg and 29.32 g/kg. Conclusions The effect of the combined administration of Bletilla striata and Radix aconiti preparata showed relationship among the doses and ratios on anhydrous ethanol-induced gastric mucosal injury in mice with gastric ulcer. Key words: Eighteen clashes; Radix aconiti preparata; Bletilla striata; Stomach ulcer; Mice

Protective Effect of Camellia Oil (Camellia oleifera Abel.) against Ethanol-Induced Acute Oxidative Injury of the Gastric Mucosa in Mice.

Camellia oil, a common edible oil in Taiwan and China, has health effects for the gastrointestinal tract in folk medicine, and it contains abundant unsaturated fatty acids and phytochemicals. However, the preventive effect of camellia oil on ethanol-induced gastric ulcers remains unclear. This study was aimed to evaluate the preventive effect of camellia oil on ethanol-induced gastric injury in vitro and in vivo as well as its mechanisms of action. In an in vitro study, our results showed that pretreatment of RGM-1 cells with camellia oil enhanced the migration ability as well as increased heat shock protein expression and reduced apoptotic protein expression. In animal experiments, mice pretreated with camellia oil effectively showed improved ethanol-induced acute injury of the gastric muscosa and oxidative damage through the enhancement of antioxidant enzyme activities and heat shock protein and PGE2 production, as well as the suppression of lipid peroxidation, apoptosis-related proteins, pro-inflammatory cytokines, and NO production. Histological injury score and hemorrhage score in ethanol-induced gastric mucosal damage dramatically elevated from the control group (0.00 ± 0.0) to 3.40 ± 0.7 and 2.60 ± 0.5, respectively. However, treatments with camellia oil or olive oil (2 mL/kg bw) and lansoprazole (30 mg/kg bw) showed significant decreases in elevation of injury score and hemorrhage score (p < 0.05). Therefore, camellia oil has the potential to ameliorate ethanol-induced acute gastric mucosal injury through the inhibition of inflammation and oxidative stress.

Protective effects of hot spring water drinking and radon inhalation on ethanol-induced gastric mucosal injury in mice.

ABSTRACTRadon therapy using radon (222Rn) gas is classified into two types of treatment: inhalation of radon gas and drinking water containing radon. Although short- or long-term intake of spa water is effective in increasing gastric mucosal blood flow, and spa water therapy is useful for treating chronic gastritis and gastric ulcer, the underlying mechanisms for and precise effects of radon protection against mucosal injury are unclear. In the present study, we examined the protective effects of hot spring water drinking and radon inhalation on ethanol-induced gastric mucosal injury in mice. Mice inhaled radon at a concentration of 2000 Bq/m3 for 24 h or were provided with hot spring water for 2 weeks. The activity density of 222Rn ranged from 663 Bq/l (start point of supplying) to 100 Bq/l (end point of supplying). Mice were then orally administered ethanol at three concentrations. The ulcer index (UI), an indicator of mucosal injury, increased in response to the administration of ethanol; however, treatment with either radon inhalation or hot spring water inhibited the elevation in the UI due to ethanol. Although no significant differences in antioxidative enzymes were observed between the radon-treated groups and the non-treated control groups, lipid peroxide levels were significantly lower in the stomachs of mice pre-treated with radon or hot spring water. These results suggest that hot spring water drinking and radon inhalation inhibit ethanol-induced gastric mucosal injury.

Gastroprotective effect of gamma-aminobutyric acid against ethanol-induced gastric mucosal injury

The present study aimed to investigate the gastroprotective effect of gamma-aminobutyric acid (GABA) on ethanol-induced gastric mucosal injury and gastric epithelial cells injury. Rats were divided into the control group, vehicle group and GABA-treated groups (10, 20 and 40 mg/kg/day). After GABA ingestion for 14 days, rats except the control group were given 1 mL pure ethanol by oral gavage in order to induce acute gastric mucosal lesion. The human gastric epithelial cell line GES-1 was incubated with GABA (100, 200 and 400 μM) for 24 h, followed by treatment with 8% ethanol for 3 h to induce cell injury. The results showed that GABA pretreatment significantly reduced gastric ulcer index in a dose-dependent manner. GABA pretreatment could not only remarkably restrain oxidative stress by increasing activities of superoxide dismutase and catalase as well as decreasing content of malondialdehyde both in gastric tissue and cells, but also significantly reduced pro-inflammatory factors (interleukin-6 and tumor necrosis factor α) levels in gastric tissue. In addition, significant augments of prostaglandin E2 and nitric oxide levels were observed in the gastric tissues of 40 mg/kg/d GABA treated group. In conclusion, the results in this study suggested that GABA could alleviate ethanol-induced gastric mucosal injury and gastric epithelial cells injury through the improvement of anti-inflammatory and anti-oxidant status, as well as the increase of PGE2 and NO levels.

EFFECTS OF THE METHANOLIC EXTRACT OF OCIMUM BASILICUM (GREEN PEAS) LEAVES ON ETHANOL-INDUCED GASTRIC MUCOSAL INJURY IN ADULT MALE ALBINO RATS

Background: There is a great interest towards the medicinal herbs as a new line of treatment with less side effects. Objective: Evaluation and standardization of the protective effect of Ocimum basilicum extract which is used as traditional medicine against ethanol-induced gastric mucosal damage. Material and Methods: Fifty adult male albino rats of local strain weighing between 150 and 185 grams were used for this study. The rats were divided into four groups, control, ethanol-treated, Ocimum basilicum plus ethanol-treated, and cimetidine plus ethanol-treated. The rats received the extract in two different dose concentrations (100 and 200 mg/kg b.w. orally), and cimetidine (100 mg/kg b.w. subcutaneously) for seven successive days. One hour later after the seventh day dose, the rats of the third and fourth groups received a single dose of 70% ethanol (1 ml/rat) orally. Results: The tested two concentrations of the extract showed a dose-dependent preventive index of 54.3% and 84.3% for the small and large dose respectively. It was noticed that the larger dose of the Ocimum basilicum extract showed a gastric mucosal protection nearly similar to that produced by cimetidine. Conclusion: Ocimum basilicum leaves extract was effective in protection of gastric mucosa against ethanol-induced gastric mucosal injury.