Camellia oil (Camellia oleifera Abel.) alleviates gastric injury induced by ethanol associated with modulation of gut microbiota in mice

Oil from Camellia oleifera Abel. seed is a popular edible oil in Asia, which has gained much attention for itsmedicinal applications on relieving various inflammation, however, the mechanism is still unknown. The presentstudy was to investigate the gastroprotective effect of camellia oil against ethanol-induced gastric mucosal injuryin mice. The results showed that camellia oil pretreatment significantly reduced gastric ulcer injury. A remarkableinhibited oxidative stress by reducing the concentration of malondialdehyde and a significant decrease of thelevels of pro-inflammatory factors in gastric tissue were observed in camellia oil pretreated group. In addition,camellia oil improved the diversity of gut microbiota and changed the community structure and composition byincreasing Bacteriodes and Dorea. And the feces metabolomics found that metabolism of cofactors and vitamins,and lipid, carbohydrate and amino acid metabolism were modulated by admiration of camellia oil. Takentogether, the findings of this study suggested that camellia oil could ease the ethanol-induced gastric mucosalinjury via the improvement of anti-oxidant and anti-inflammatory status, as well as the regulation of gutmicrobiota and its metabolites.

Lansoprazole prevents experimental gastric injury induced by non-steroidal anti-inflammatory drugs through a reduction of mucosal oxidative damage

AIM:This study investigated the mechanisms of protection afforded by the proton pump inhibitor lansoprazole against gastric injury induced by different non-steroidal anti-inflammatory drugs (NSAIDs) in rats. METHODS: Male Sprague-Dawley rats were orally treated with indomethacin (100 μmol/kg), diclofenac (60 μmol/kg), piroxicam (150 μmol/kg) or ketoprofen (150 μmol/kg). Thirty minutes before NSAIDs, animals were orally treated with lansoprazole 18 or 90 umol/kg. Four hours after the end of treatments, the following parameters were assessed: gastric mucosal PGE2, malondialdehyde (MDA), myeloperoxidase (MPO) or non-proteic sulfhydryl compounds (GSH) levels; reverse transcription-polymerase chain reaction (RT-PCR) of mucosal COX-2 mRNA; gastric acid secretion in pylorus-ligated animals; in vitro effects of lansoprazole (1-300 μmol/L) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate. RESULTS: All NSAIDs elicited mucosal necrotic lesions which were associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels were detected in the gastric mucosa of indomethacin- or piroxicam-treated animals. Indomethacin enhanced mucosal cyclooxygenase-2 expression, while not affecting cyclooxygenase-1. At the oral dose of 18 μmol/kg lansoprazole partly counteracted diclofenac-induced mucosal damage, whereas at 90 μmol/kg it markedly prevented injuries evoked by all test NSAIDs. Lansoprazole at 90 μmol/kg reversed also the effects of NSAIDs on MPO, MDA and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced cyclooxygenase-2 expression. However, both lansoprazole doses markedly inhibited acid secretion in pylorus-ligated rats. Lansoprazole concentration-dependently reduced the oxidation of LDLs in vitro. CONCLUSION: These results suggest that, besides the inhibition of acid secretion, lansoprazole protection against NSAID-induced gastric damage depends on a reduction in mucosal oxidative injury, which is also responsible for an increment of sulfhydryl radical bioavailability. It is also suggested that lansoprazole does not influence the down-regulation of gastric prostaglandin production associated with NSAID treatment.

Irsogladine maleate suppresses indomethacin-induced elevation of proinflammatory cytokines and gastric injury in rats

AIM： To investigate the mucosal protective effect and the mechanisms of action of the anti-ulcer drug irsogladine maleate in gastric injury induced by indomethacin in rats. METHODS： Gastric mucosal injury was induced in male Hos：Donryu rats by oral administration of indomethacin at a dose of 48 mg/kg. One hour before indomethacin treatment, animals were orally pretreated with irsogladine maleate at doses of 1 mg/kg, 3 mg/kg or 10 mg/kg. Four hours after indomethacin administration, the animals were sacrificed and their stomachs were rapidly removed and processed for the evaluation of gastric mucosal damage and the determination of the concentrations of tumor necrosis factor-α （TNF-α）, interleukin-1β （IL-1β）, IL-8 and myeloperoxidase （MPO） in mucosal tissues. RESULTS： Linear hemorrhagic mucosal lesions were observed primarily in the glandular stomach 4 h alter oral administration of indomethacin. Pretreatment with irsogladine maleate markedly reduced the number and severity of these lesions in a dose-dependent manner. The mucosal concentrations of proinflammatory cytokines （TNF-α, IL-1β, and IL-8） and MPO, which indicates the degree of mucosal infiltration by neutrophils, increased concomitantly with the occurrence of gastric injury in the indomethacintreated rats. Pretreatment with irsogladine maleate significantly decreased the levels of these inflammatory factors in gastric tissue elicited by indomethacin.CONCLUSION： The mucosal protective effects afforded by irsogladine maleate on gastric injury induced by indomethacin are mediated by inhibition of mucosal proinflammatory cytokine production and neutrophil infiltration, leading to suppression of mucosal inflammation and subsequent tissue destruction.

Aloe vera attenuated gastric injury on indomethacin-induced gastropathy in rats

AIM: To evaluate the protective effects of Aloe vera on gastric injury in rats with indomethacin (IMN)-induced gastropathy.

Endoscopic and histopathological evaluation of acute gastric injury in high-dose acetaminophen and nonsteroidal anti-inflammatory drug ingestion with suicidal intent

AIM： To evaluate endoscopic and histopathologic aspects of acute gastric injury due to ingestion of high-dose acetaminophen and nonsteroidal antiinflammatory drugs （NSAIDs） with respect to some risk factors and patient characteristics. METHODS： The study group consists of 50 patients admitted to emergency department with high dose analgesic ingestion （group Ⅰ ） with suicidal intent. Thirty patients with or without mild complaints of dyspepsia （group Ⅱ） were selected as the control group. The study group was stratified according to the use of type and number of analgesics. Endoscopic findings were evaluated according to the Lanza score （LS）, expressing the severity of the gastroduodenal damage and biopsies according to a scoring system based on histopathologic findings of acute erosive gastritis. RESULTS： Gastroduodenal damage was significantly more severe in group Ⅰ compared to group Ⅱ （P 〈 0.01）. The LS was similar in both groups Ⅰ a and Ⅰb. However LS was significantly higher in patients who had ingested multiple NSAIDs （group Ⅰ c） compared to other patients （P 〈 0.01）. The LS was correlated to age （P 〈 0.01） and total amount of drug ingested （P 〈 0.05） in group Ⅰ ; but it was not correlated with Helicobacter pylori （H pylori） infection or duration of exposure （P 〉 0.05）. The biopsy score （BS） was higher in group Ⅰ than group Ⅱ （P 〈 0.01）, and higher in group Ⅰb than group Ⅰa （P 〈 0.05）. CONCLUSION： The histopathologic damage was more severe among NSAID ingesting patients compared to those ingesting only acetaminophen and there is no significant difference in the endoscopic findings between the groups. There is no significant difference in the LS between the groups. This lack of significance is remarkable in terms of the gastric effects of highdose acetaminophen.

Ligustrazine alleviates gastric mucosal injury in a rat model of acute necrotizing pancreatitis

BACKGROUND: Acute necrotizing pancreatitis (ANP) leads to a systemic inflammatory response characterized by widespread leukocyte activation and, as a consequence, distant organ injury. The aim of this study was to explore the relationship between gastric microcirculatory impairment and inflammatory mediators released in rats and to evaluate the therapeutic effect of ligustrazine extracted from Rhizoma ligusticum wallichii on gastric mucosa injury in a rat model of ANP. METHODS: Ninety-six Sprague-Dawley rats were randomly divided into three groups: normal control (group Q; ANP without treatment (group P); and ANP treated with ligustrazine (group T). The ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane (4 ml/kg). Group C was given isovolumetric injection of 9 g/L physiological saline by the same route. Group T was injected with ligustrazine (10 ml/kg) via the portal vein. The radioactive biomicrosphere technique was used to measure the blood flow 2 and 12 hours after the induction of ANP. Samples of the pancreas and stomach were taken to assess pathological changes by a validated histology score; meanwhile, the levels of serum interleukin-1 beta (IL-1 beta) were determined. Gastric tissues were also used to measure the level of myeloperoxidase (MPO), which is expressed intracellularly in the azurophilic granules of neutrophils. RESULTS: Blood flow in group P was significantly lower than that in group C (P < 0.01). Pathological changes were significantly aggravated in group P. The gastric MPO activity in group P was significantly higher than that in group C (P < 0.01). The level of serum IL-1 beta in group P increased more significantly than that in group C (P < 0.01). Blood flow of the stomach in group T was significantly higher than that in group P after 2 hours (P < 0.01). The pathological changes were significantly alleviated in group T. The MPO activity of group T was significantly lower than that of group P (P < 0.01). Although serum IL-1 beta level of group T, was higher than of group C (P < 0.01), it was lower than that of group P (P < 0.01). There was a negative correlation between gastric blood flow and MPO activity (r=-0.983, P < 0.01), and between gastric blood flow and pathological score (r=-0.917, P < 0.05). CONCLUSIONS: Decreased gastric blood flow and increased inflammatory mediators can be seen early in ANP, and both are important factors for gastric and mucosal injury. Ligustrazine can ameliorate microcirculatory disorder and alleviate the damage to the pancreas and stomach.

Effect of acupuncture at different meridian acupoints on changes of related factors for rabbit gastric mucosal injury

AIM： To explore the regularity of multi-meridians controlling a same viscus （MMCSV）. METHODS： The rabbit gastric ulcer model was established by ethanol intragastric instillation. Fifty-six rabbits were randomly divided into normal group, model group （MG）, model plus acupuncture at Foot Yangming Meridian group （YMG）, model plus acupuncture at Foot Taiyin Meridian group （TYG）, model plus acupuncture at Foot Shaoyang Meridian group （SYG）, model plus acupuncture at Foot Jueyin Meridian group （JYG）, model plus acupuncture at Foot Taiyang Meridian group （TYMG）, with eight rabbits in each group. Gastric mucosal nitric oxide （NO） and nitric oxide synthase （NOS） were assayed by the nitric acid reductase method, and prostaglandin E2 （PGE2） and epidermal growth factor （EGF） were measured by radioimmunoassay. The comprehensive effects were analyzed by weighing method. RESULTS： Compared to MG, SYG, JYG and TYMG, the rabbits gastric mucosal injury index （GMII） reduced very significantly in YMG （P〈0.01）. Compared to MG, the GMII also reduced significantly in TYG （P〈0.05）. NO, NOS, PGE2 and EGF increased very significantly in YMG （P〈0.01）. The EGF in YMG also increased significantly than that in TYG compared to those in MG, SYG, JYG and TYMG （P〈0.05）. The PGE2 and EGF also increased very significantly in TYG than those in MG, JYG and TYMG （P〈0.01）. While compared to SYG, the NOS increased significantly in TYG （P〈0.05）. NOS was the highest in YMG （P〈0.01）, and was higher in TYG than in MG （P〈0.01）. CONCLUSION： MMCSV is common. The Foot Yangming Meridian is most closely related to the stomach, followed by Foot Taiyin Meridian, Foot Shaoyang Meridian and Foot Jueyin Meridian. Foot Taiyang Meridian has no correlation with the stomach.

Hydrogen sulfide attenuates gastric mucosal injury induced by restraint water-immersion stress via activation of KATPchannel and NF-κB dependent pathway

AIMTo explore the effect of hydrogen sulfide (H2S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway on such an effect.METHODSMale Wistar rats were randomly divided into a control group, a physiological saline (PS) group, a sodium hydrosulfide (NaHS) group, a glibenclamide (Gl) group, Gl plus NaHS group, a pyrrolidine dithiocarbamate (PDTC) group, and a PDTC plus NaHS group. Gastric mucosal injury was induced by RWIS for 3 h in rats, and gastric mucosal damage was analyzed after that. The PS, NaHS (100 μmol/kg body weight), Gl (100 μmol/kg body weight), Gl (100 μmol/kg or 150 μmol/kg body weight) plus NaHS (100 μmol/kg body weight), PDTC (100 μmol/kg body weight), and PDTC (100 μmol/kg body weight) plus NaHS (100 μmol/kg body weight) were respectively injected intravenously before RWIS.RESULTSRWIS induced serious gastric lesions in the rats in the PS pretreatment group. The pretreatment of NaHS (a H2S donor) significantly reduced the damage induced by RWIS. The gastric protective effect of the NaHS during RWIS was attenuated by PDTC, an NF-κB inhibitor, and also by glibenclamide, an ATP-sensitive potassium channel blocker, in a dose-dependent manner.CONCLUSIONThese results suggest that exogenous H2S plays a protective role against RWIS injury in rats, possibly through modulation of KATP channel opening and the NF-κB dependent pathway.

Total triterpenes from fruits of Chaenomeles speciosa(Sweet) Nakai protect against indomethacin-induced gastric mucosal injury: involvement of TFF1-mediated EGF/EGFR and apoptotic pathways

OBJECTIVE Gastric ulcers affect people of all ages and half of the world's population,which is being considered as the new"plague of the 21st century".As is well known,gastric mucosa is known as the first guard to protect the stomach from ulcer injury,while the aetiology of gastric ulcer is relative to imbalances between gastric mucosal protective and aggressive factors.Therefore,reducing or eliminating the aggressive factors,returning to the balance of between mucosal protective and aggressive factors,and then restoring the normal functional of gastric mucosal barrier could be crucial for treating the gastric ulcer.The fruits of Chaenomeles speciosa(TCS),also known as"mugua",might be processed into edible and health care derived products,and used as a commonly used traditional medicine in China for thousands of years.In China folk,there is a saying that"apricot one benefit,pear two benefits,mgua hundred benefits",so it has a"hundred-benefit"fruit reputation.Tujia nationality inhabitants in Southwestern China should have rheumatic diseases and peptic ulcers for living in the damp environments and bingeing on spicy and pungent foods.For the exis⁃tence of the fruit derived products of Chaenomeles speciosa as their complementary foods or snacks,the habit makes them rarely suffer from the two kinds of diseases.Enlightened by these,we had investigated the structure-activity rela⁃tionships,screened out CSTT with gastroprotective activity.Our previous studies demonstrated that TCS owned effec⁃tively therapeutic effects on gastric ulcer patients and animals,and further confirmed that TFF1 and apoptotic pathway were closely interrelated with its exerting gastroprotection.However,its underlying molecular mechanisms involved have not been fully elucidated.The current study was to further investigate its protective effect on indomethacin(IND)-damaged RGM-1 cells and rats and its underlying mechanisms through modulating TFF1-mediated EGF/EGFR and apoptotic pathways.METHODS The gastroprotection of TCS was evaluated with IND-induced gastric lesions model in RGM-1 cells and rats.In vitro,the proliferation,migration,mitochondrial viability and apoptosis were assessed,In vivo,ulcer index,ulcer inhibition rate,gastric juice acidity,gastric wall mucus(GWM),histopathology of gastric mucosa were detected.The gastroprotective effects of TCS through the TFF1-mediated EGFR/EGFR and apoptotic pathways were presented and measured by qRT-PCR and Western blotting assays.RESULTS TCS had gastroprotective function,which was related to the amelioration in promoting IND-damaged RGM-1 cell proliferation and migration,hoisting gastric juice acidity and GWM,improving ulcer index and ulcer inhibition rate,attenuating the hemorrhage,edema,epithelial cell loss and inflammatory cell infiltration of gastric mucosa,upregulating proliferation cell nuclear antigen,Bcl-2,Bcl-xl mRNA and TFF1,EGF,p-EGFR,p-Src,pro-caspase-3,pro-caspase-9 protein expressions,mitochondrial viability,mitochondrial cytochrome C concentration and p-EGFR/EGFR,p-Src/Src,Bcl-2/Bax,Bcl-xl/Bad ratioes,downregulating Bax,Bad,Apaf-1 mRNA and cleaved-caspase-3,cleaved-caspase-9,cleaved-PARP-1 protein expressions,cytosol cytochrome C concentration.CONCLUSION TCS′s gastroprotective effect was closely connected with boosting TFF1 expression,acti⁃vating TFF1-mediated EGF/EGFR pathway,thus restraining mitochondrial-dependent apoptosis,which provided new insights into interpreting its underlying mechanism and promised to act as a candidate drug to treat gastric mucosal injury.

EFFECT OF ELECTROACUPUNCTURE OF "ZUSANLI" ON VIP CONTENTS OF THE PERIPHERAL BLOOD, GASTRIC MUCOSAL AND BRAIN TISSUES IN GASTRIC MUCOSAL INJURY RATS

Objective: To observe the therapeutic effect of electroacupuncture (EA) of "Zusanli"(ST 36) on vasoactive intestinal peptide (VIP) levels in the peripheral blood, gastric mucosal and brain tissues in experimental gastric injury rats. Methods: Gastric mucosal injury model was established by using cold restraining stress method. 40 Wistar rats were randomly and evenly divided into normal control group, model group, EA group and non acupoint group. VIP contents of plasma and gastric mucosal and medulla oblongata tissues were assayed using radioimmunoassay and gastric mucosal blood flow (GMBF) was measured by employing hydrogen clearing method. Results: In cold restraining stress rats, spot and strip like bleeding necrosis foci in the gastric mucous primarily in the gastric antrum could be seen clearly, GMBF and VIP contents in plasma, gastric mucous and brain tissues declined significantly (P<0.05, 0.01), while the gastric mucosal lesion index (LI) raised significantly (P<0.05) in comparison with those of normal control group. Following EA of "Zusanli" (ST 36), GMBF decreased pronouncedly, VIP contents of the plasma, bulba and gastric mucosal tissues increased strikingly in comparison with model group (P<0.01). Conclusion: EA of "Zusanli" (ST 36) possesses a protection effect on gastric mucous under stress condition and VIP is involved in the effect of EA.

Protective role of fruits of Rosa odorata var. gigantea against WIRSinduced gastric mucosal injury in rats by modulating pathway related to inflammation, oxidative stress and apoptosis

Objective: Rosa odorata var. gigantea is a popular medicinal plant. Some studies have demonstrated that ethanolic extract of the fruits of R. odorata var. gigantea(FOE) has gastroprotective properties. The aim of this study was to investigate the gastroprotective activity of FOE on water immersion restrained stress(WIRS)-induced gastric mucosal injury in a rat model and elucidate the possible molecular mechanisms involved.Methods: A rat stress ulcer model was established in this study using WIRS. After rats were treated with FOE orally for 7 d, the effect of FOE treatment was analyzed by hematoxylin and eosin(H&E) staining, and the changes of inflammatory factors, oxidative stress factors, and gastric-specific regulatory factors and pepsin in the blood and gastric tissues of rats were examined by ELISA assay. Molecular mechanism of FOE was investigated by immunohistochemical assay and Western blot.Results: Compared with the WIRS group, FOE could diminish both the macroscopic and microscopic pathological morphology of gastric mucosa. FOE significantly preserved the antioxidants glutathione peroxidase(GSH-PX), superoxide dismutase(SOD) and catalase(CAT) contents;anti-inflammatory cytokines interleukin-10(IL-10) and prostaglandin E2(PGE2) levels as well as regulatory factors tumor necrosis factor-a(TGF-a) and somatostatin(SS) contents, while decreasing malondialdehyde(MDA), nitric oxide synthase(i NOS), tumor necrosis factor(TNF-a), interleukin-1β(IL-1β), interleukin-6(IL-6), gastrin(GAS)and endothelin(ET) levels. Moreover, FOE distinctly upregulated the expression of Nrf2, HO-1, Bcl2 and proliferating cell nuclear antigen(PCNA). In addition, FOE activated the expression of p-EGFR and downregulated the expression of NF-ΚB, Bax, Cleaved-caspase-3, Cyto-C and Cleaved-PARP1, thus promoting gastric mucosal cell survival.Conclusion: The current work demonstrated that FOE exerted a gastroprotective activity against gastric mucosal injury induced by WIRS. The underlying mechanism might be associated with the improvement of anti-inflammatory, anti-oxidation and anti-apoptosis systems.

Attenuation of gastric mucosal inflammation induced by aspirin through activation of A_(2A) adenosine receptor in rats

AIM： To determine whether a specific adenosine A2A receptor agonist （ATL-146e） can ameliorate aspirin-induced gastric mucosal lesions in rats, and reduce neutrophil accumulation and production of pro-inflammatory cytokines. METHODS： Gastric lesions were produced by oral gavage of aspirin （200 mg/kg） and HCI （0.15 mol/L, 8.0 mL/kg）. 4-{3-[6-Amino-9-（5-ethylcarbamoyl-3,4- dihydroxy-tetrahydro-furan-2-yl）-9H-purin-2-yl]-prop-2- ynyl}-cyclohexanecarboxylic acid methyl ester （ATL-146e, 2.5-5μg/kg, IP） was injected 30 min before the administration of aspirin. Tissue myeloperoxidase （MPO） concentration in gastric mucosa was measured as an index of neutrophil infiltration. Gastric mucosal concentrations of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） were determined by ELISA. Also, we examined the effect of ATL-146e on tissue prostaglandin E2 （PGE2） production and gastric secretion. RESULTS： Intragastric administration of aspirin induced multiple hemorrhagic erosions in rat gastric mucosa. The total length of gastric erosions （ulcer index） in control rats was 29.8±7.75 mm and was reduced to 3.8±1.42 mm alter pretreatment with 5.0 g/kg ATL-146e （P〈 0.01）. The gastric contents of MPO and pro-inflammatory cytokines were all increased after the administration of aspirin and reduced to nearly normal levels by ATL-146e. Gastric mucosal PGE2 concentration was not affected by intraperitoneal injection of ATL-146e. CONCLUSION： The specific adenosine A2A receptor agonist, ATL-146e, has potent anti-ulcer effects presumably mediated by its anti-inflammatory properties.

Gastric laceration after cardiopulmonary resuscitation:A case report

The cardiopulmonary resuscitation (CPR) persists as the best practice to maintain cerebral and coronary perfusion after cardiac arrest. Due to the chest compressions and ventilation maneuvers during resuscitation, there are common complications reported. Abdominal organs injuries occur in approximately 30% of patients, although studies show that they are under diagnosticated. The aim of this article is to report a case of massive digestive hemorrhage by gastric laceration after cardiopulmonary resuscitation, due to the event severity and rare clinic diagnostic. A 75-year-old Caucasian man suffered a sudden malaise and cardiac arrest and transferred to an Emergency Unit (EU). The set of measures recommended by Advanced Cardiac Life Support (ACLS) was performed. Despite no resistance to the passage of nasogastric survey and spontaneous healing of fresh blood exteriorization, an endoscopy showed ulcers in gastric notch with clots adhered and active blood. There was no track record of liver or gastrointestinal diseases on this patient, identifying a gastric laceration after cardiopulmonary resuscitation. The mechanism by which the gastric laceration after CPR occurred is uncertain. Nevertheless, some precipitating factors are considered such as positioning of the patient during CPR, ideal point of compressions and ventilation pressure. In conclusion, this event is rare with a hard diagnostic however that could be avoided and minimized with preventive measures.

Reversing gastric mucosal alterations during ethanol-induced chronic gastritis in rats by oral administration of Opuntia ficus-indica mucilage

AIM： To study the effect of mucilage obtained from cladodes of Opuntia ficus-indica （Cactaceae） on the healing of ethanol-induced gastritis in rats. METHODS： Chronic gastric mucosa injury was treated with mucilage （5 mg/kg per day） after it was induced by ethanol. Lipid composition, activity of 5＇-nucleotidase （a membrane-associated ectoenzyme） and cytosolic activities of lactate and alcohol dehydrogenases in the plasma membrane of gastric mucosa were determined. Histological studies of gastric samples from the experimental groups were included. RESULTS： Ethanol elicited the histological profile of gastritis characterized by loss of the surface epithelium and infiltration of polymorphonuclear leukocytes. Phosphatidylcholine （PC） decreased and cholesterol content increased in plasma membranes of the gastric mucosa. In addition, cytosolic activity increased while the activity of alcohol dehydrogenases decreased. The administration of mucilage promptly corrected these enzymatic changes. In fact, mucilage readily accelerated restoration of the ethanol-induced histological alterations and the disturbances in plasma membranes of gastric mucosa, showing a univocal anti-inflammatory effect. The activity of 5＇-nucleotidase correlated with the changes in lipid composition and the fluidity of gastric mucosal plasma membranes. CONCLUSION： The beneficial action of mucilage seems correlated with stabilization of plasma membranes of damaged gastric mucosa. Molecular interactions between mucilage monosaccharides and membrane phospholipids, mainly PC and phosphatidylethanolamine （PE）, may be the relevant features responsible for changing activities of membrane-attached proteins during the healing process after chronic gastric mucosal damage.

Protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats

Objective:To observe the protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats.Methods:All rats were randomly divided into normal control group,cirrhosis and treatment group.Thioacetamide was used to establish rat model of cirrhotic portal hypertension.The necrotic tissue of gastric mucosa ulcer focus,degree of neutrophils infiltration at the ulcer margin,portal pressure,portal venous flow,abdominal aortic pressure,abdominal aortic blood flow at front end,gastric mucosal blood flow（GMBF）,glycoprotein（GP）of gastric mucosa,basal acid secretion,H’ back-diffusion,gastric mucosal damage index,NO,prostaglandin E2（PGE2） and tumor necrosis factor-α（TNF-α） were determined respectively,and the pathological changes of gastric mucosa were also observed by microscope.Results:Compared with cirrhosis group and the control group,the ulcer bottom necrotic material,gastric neutrophil infiltration and UI of the treatment group were all decreased significantly（P【0.01）,GMBF value,GP values,serum NO,PGE2,TNF- a were all significantly increased.Conclusions:Omeprazole has an important protective effect on gastric mucosal and it can increase gastric mucosal blood flow and related to many factors.

Gastric blunt traumatic injuries: A computed tomography grading classification

AIM To produce a radiological grading of gastric traumatic injuries. METHODS In our study, we retrospectively analyzed 32 cases of blunt gastric traumatic injuries and compared computed tomography(CT) data with patients' surgical or medical development. In all cases, a basal phase was acquired, and an intravenous contrast material was administered via an antecubital venous catheter with acquisition in the venous phase(70-90 s). In addition, a further set of delayed scans was performed 4-5 min after the first scanning session, without supplementary intravenous contrast material, to identify or better define areas of active bleeding. All CT examinations were retrospectively reviewed by two radiologists, with more than 5 years of experience in emergency radiology, to detect signs of gastric injuries and/or associated abdominal lesions according to literature data. Specific CT findings for gastric rupture include luminal content extravasation and discontinuity of the gastric wall, while CT findings suggestive of injury consisted of free peritoneal fluid, extraluminal air, pneumatosis, and thickening and hematoma of gastric wall.RESULTS We found 32 gastric traumatic injuries. In 22 patients(68.8%), the diagnosis was based on the surgical findings; in the other 10 patients(31.2%), the diagnosis was based on the clinical and CT radiological data. We observed discontinuity of the gastric wall and luminal content extravasation in 1 patient(3.1%); in 10 patients(31.2%), there was extra-luminal air in the peritoneum. In 28 patients(87.5%), there was peritoneal fluid, which was blood in 14 patients(hematoma in 11 patients and contrast material extravasation from active bleeding in 3 patients). In 15 patients(46.9%), there was gastric wall thickening. In 3 patients, it was possible to identify a prevalent involvement of the external layer of the gastric wall, whereas, in 2 patients, the inner side of the gastric wall presented with major involvement. In 3 patients(9.4%), pneumatosis of the gastric wall was detected. In 19(59.4%) patients, the stomach was full. The fundus was the most frequently damaged part of the stomach because it was involved in 17 patients(53.1%). Based on the observed data, we identified four grades of gastric lesions.CONCLUSION A radiologic score is helpful for guiding the diagnosis and management(surgical or conservative) of gastric blunt traumatic injuries and stratify patients according to short-term outcomes.

Study of Clinical and Genetic Risk Factors for Aspirin-inducec Gastric Mucosal Injury

Background： Current knowledge about clinical and genetic risk factors for aspirin-induced gastric mucosal injury is not sufficient to prevent these gastric mucosal lesions. Methods： We recruited aspirin takers as the exposed group and healthy volunteers as the control group. The exposed group was categorized into two subgroups such as subgroup A as gastric mucosal injury diagnosed by gastroscopy, including erosion, ulcer or bleeding of the esophagus, stomach, or duodenum; subgroup B as no injury of the gastric mucosa was detected by gastroscopy. Clinical information was collected, and 53 single nucleotide polymorphisms were evaluated. Results： Among 385 participants, 234 were in the aspirin-exposed group. According to gastroscopy, 82 belonged to subgroup A, 91 belonged to subgroup B, and gastroscopic results of 61 participants were not available. Using the Chi-square test and logistic regression, we found that peptic ulcer history （odds ratio [OR] = 5.924, 95% confidence intervals [C/]： 2.115-16.592）, dual anti-platelet medication （OR = 3.443, 95% CI： 1.154-10.271 ）, current Helicobacterpylori infection （OR = 2.242, 95% CI： 1.032-4.870）, male gender （OR = 2.211, 95% CI： 1.027-4.760）, GG genotype ofrs2243086 （OR = 4.516, 95% CI： I. 180-17.278）, and AA genotype ofrs 1330344 （OR = 2.178, 95% CI： 1.016-4.669） were more frequent in subgroup A than subgroup B. In aspirin users who suffered from upper gastrointestinal bleeding, the frequency of the TT genotype ofrs2238631 and TT genotype ofrs2243100 was higher than in those without upper gastrointestinal bleeding. Conclusions： Peptic ulcer history, dual anti-platelet medication, tt. pylori current infection, and male gender were possible clinical risk factors for aspirin-induced gastric mucosal injury. GG genotype of rs2243086 and AA genotype of rs 1330344 were possible genetic risk factors. TT genotype ofrs2238631 and TT genotype ofrs2243100 may be risk factors for upper gastrointestinal bleeding in aspirin users.

Effect of Weikang Capsule(胃康胶囊)on Aspirin-Related Gastric and Small Intestinal Mucosal Injury

Objective To investigate the effects of Weikang Capsule(胃康胶囊,WKC)on aspirin-related gastric and small intestinal mucosal injury by magnetically controlled capsule endoscopy(MCCE).Methods Patients taking enteric-coated aspirin aged 40-75 years were enrolled in Beijing Anzhen Hospital,Capital Medical University from January 2019 to December 2019.The patients continued taking aspirin Tablet(100 mg per day)and underwent MCCE before and after 1-month combined treatment with WKC(0.9 g per time orally,3 times per day).The gastrointestinal symptom score,gastric Lanza score,the duodenal,jejunal and ileal mucosal injury scores were used to evaluate the gastrointestinal injury before and after treatment.Adverse events including nausea,vomiting,abdominal pain,abdominal distension,abdominal discomfort,dizziness,or headache during MCCE and combined treatment were observed and recorded.Results Twenty-two patients(male/female,13/9)taking enteric-coated aspirin aged 59.5±11.3 years with a duration of aspirin use of 28.0(1.0,48.0)months were recruited.Compared with pre-treatment,the gastrointestinal symptom rating scale scores,gastric Lanza scores,and duodenal mucosal injury scores were significantly reduced after 1-month WKC treatment(P<0.05),and jejunal and ileal mucosal injury scores showed no obvious change.No adverse events occurred during the trial.Conclusions WKC can alleviate gastrointestinal symptoms,as well as gastric and duodenal mucosal injuries,in patients taking enteric-coated aspirin;it does not aggravate jejunal or ileal mucosal injury,which may be an effective alternative for these patients(Clinical trial registry No.ChiCTR1900025451).