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

2020 ◽  
Vol 45 (7) ◽  
pp. 731-736 ◽  
Author(s):  
Mervat S. Taha ◽  
Emad. M. El-Sherbiny ◽  
Hala. F. Osman
Keyword(s):  
Drinking Water ◽  
Gastric Mucosa ◽  
Total Protein ◽  
Gum Arabic ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
Ethanol Administration ◽  
Albino Rats ◽  
Tnf Α ◽  
Ulcerogenic Activity

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.

Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production

2008 ◽  
Vol 294 (1) ◽  
pp. G80-G87 ◽  
Author(s):  
Youichiro Hattori ◽  
Takashi Ohno ◽  
Takako Ae ◽  
Takeo Saeki ◽  
Katsuharu Arai ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Protective Action ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
Ethanol Administration ◽  
Receptor Subtypes ◽  
Receptor Signaling ◽  
Mucosal Protection ◽  
Anesthetized Rats ◽  
Gastric Mucosal Protection

Prostaglandin (PG)E derivatives are widely used for treating gastric mucosal injury. PGE receptors are classified into four subtypes, EP1, EP2, EP3, and EP4. We have tested which EP receptor subtypes participate in gastric mucosal protection against ethanol-induced gastric mucosal injury and clarified the mechanisms of such protection. The gastric mucosa of anesthetized rats was perfused at 2 ml/min with physiological saline, agonists for EP1, EP2, EP3, and EP4, or 50% ethanol, using a constant-rate pump connected to a cannula placed in the esophagus. The gastric microcirculation of the mucosal base of anesthetized rats was observed by transillumination through a window made by removal of the adventitia and muscularis externa. PGE2 and subtype-specific EP agonists were applied to the muscularis mucosae at the window. Application of 50% ethanol dilated the mucosal arterioles and constricted the collecting venules. Collecting venule constriction by ethanol was completely inhibited by PGE2 and by EP2 and EP4 agonists (100 nM) but not by an EP1 or an EP3 agonist. Ethanol-induced mucosal injury was also inhibited by EP2 and EP4 agonists. When leukotriene (LT)C4 levels in the perfusate of the gastric mucosa were determined by ELISA, intragastric ethanol administration elevated the LTC4 levels sixfold from the basal levels. These elevated levels were significantly (60%) reduced by both EP2 and EP4 agonists but not by other EP agonists. Since LTC4 application at the window constricted collecting venules strongly, and an LTC antagonist reduced ethanol-induced mucosal injury, reductions in LTC4 generation in response to EP2 and EP4 receptor signaling may be relevant to the protective action of PGE2. The present results indicate that EP2 and EP4 receptor signaling inhibits ethanol-induced gastric mucosal injury through cancellation of collecting venule constriction by reducing LTC4 production.

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

2014 ◽  
Vol 54 (1-2) ◽  
pp. 75-86 ◽  
Author(s):  
Hagen Bomberg ◽  
Benjamin Bierbach ◽  
Stephan Flache ◽  
Matous Novák ◽  
Doris Bandner-Risch ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiopulmonary Bypass ◽  
Gastric Mucosa ◽  
Apoptotic Cell ◽  
Mucosal Injury ◽  
Apoptotic Cell Death ◽  
Gastric Mucosal Injury ◽  
Receptor Subtypes ◽  
Leukocytic Infiltration ◽  
Group I

Background/Aim: Upper gastrointestinal bleeding (UGIB) is one of the most frequent gastrointestinal complications after cardiac surgery with cardiopulmonary bypass (CPB). Endothelin expression and microcirculatory dysfunction have been shown to be involved in UGIB. The aim of this study was to analyze the effect of vasopressin during CPB on the gastric mucosal microcirculation and the involvement of the endothelin system. Methods: Eighteen pigs were randomized into three groups (n = 6 each): group I = sham, group II = CPB (1-hour CPB) and group III = CPB + vasopressin (1-hour CPB and vasopressin administration during CPB to maintain baseline arterial pressure). All animals were observed for a further 90 min after termination of CPB. Systemic hemodynamics as well as blood flow and oxygen saturation of the gastric mucosa were measured continuously. At the end of the experiment, the gastric mucosal expressions of endothelin-1 (ET-1) and its receptor subtypes A (ETA) and B (ETB) were determined by polymerase chain reaction. Gastric mucosal injury, apoptotic cell death and leukocytic infiltration were determined by histology and immunohistochemical analyses of cleaved caspase-3 and myeloperoxidase. Results: CPB decreased gastric microvascular perfusion, which was associated with an increased expression of ET-1 and ETA. Vasopressin aggravated the CPB-associated malperfusion, whereas it completely abrogated the upregulation of ET-1 and ETA. Interestingly, vasopressin did not induce gastric mucosal morphologic injury, leukocytic infiltration or apoptotic cell death. Conclusion: Vasopressin aggravates CPB-associated microvascular malperfusion of the gastric mucosa but does not induce gastric mucosal injury.

Role of endogenous nitric oxide synthase inhibitor in gastric mucosal injury

2008 ◽  
Vol 86 (3) ◽  
pp. 97-104 ◽  
Author(s):  
Li Wang ◽  
Yuan Zhou ◽  
Jun Peng ◽  
Zhe Zhang ◽  
De-Jian Jiang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
Epithelial Cell Line ◽  
Tnf Α ◽  
Endogenous Nitric Oxide ◽  
Injury Models ◽  
Oxide Synthase

To explore the role of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA) in gastric mucosal injury, 3 models of gastric mucosal injury induced by ethanol, indomethacin, or cold stress were used in rats. The cultured human gastric mucosal epithelial cell line GES-1 infected by Helicobacter pylori (Hp) was selected to mimic human gastric mucosal injury. Gastric mucosal ulcer index (UI), levels of ADMA and NO, and activity of dimethylarginine dimethylaminohydrolase (DDAH) were determined in the mucosal injury models; in Hp-infected or ADMA-treated GES-1 cells, levels of ADMA, NO, and TNF-α and activity of DDAH were measured. The results showed that UI and levels of ADMA were markedly increased and accompanied by significantly decreased DDAH activity in the mucosal injury models. Incubation of GES-1 cells with Hp increased levels of TNF-α and ADMA and decreased activity of DDAH. Administration of ADMA also increased levels of TNF-α. The results suggest that ADMA plays an important role in facilitating gastric mucosal injury, an effect which is associated with inhibiting NO synthesis and inducing inflammatory reaction.

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

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Likang Wang ◽  
Wei Chen ◽  
Xisheng Lin ◽  
Zhao Zhang ◽  
Na Wang ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Gastric Mucosa ◽  
Protective Effect ◽  
Chronic Gastritis ◽  
Reduced Glutathione ◽  
Lipid Peroxide ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
Inflammatory Factors ◽  
Ultraviolet C

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

Nitric oxide synthase induction and cytoprotection of rat gastric mucosa from injury by ethanol

1994 ◽  
Vol 72 (11) ◽  
pp. 1308-1312 ◽  
Author(s):  
B. L. Tepperman ◽  
B. D. Soper
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Mucosal Injury ◽  
Mucosal Damage ◽  
No Synthase ◽  
Ethanol Administration ◽  
Ethanol Treatment ◽  
Concurrent Administration ◽  
Rat Gastric Mucosa ◽  
Synthase Inhibitor

The present study determined the effects of nitric oxide (NO) synthase induction on ethanol-mediated damage to rat gastric mucosa. NO synthase activity was determined by [14C]arginine conversion to radiolabeled citrulline. Ca2+-independent NO synthase activity was determined by citrulline formation in the presence of EGTA (1 mM) in the incubation mixture. Intraluminal ethanol administration (2 mL; 40% w/v) to control rats resulted in an increase in mucosal damage characterized as vasocongestion and hemorrhagic necrosis and a reduction in Ca2+-dependent NO synthase activity. Administration of Escherichia coli lipopolysaccharide (LPS; 3 mg/kg i.v.) augmented Ca2+-independent NO synthase activity (determined 4 h later) and reduced damage in response to intraluminal ethanol instillation. Ethanol treatment did not significantly affect induction of NO synthase activity. Dexamethasone pretreatment (1 mg/kg i.v. 2 h before LPS administration) reduced both Ca2+-independent NO synthase activity and the gastroprotective effect of LPS against ethanol-mediated mucosal injury. Likewise, concurrent administration of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (10 mg/kg s.c.) inhibited the gastroprotection associated with LPS treatment, an effect abolished by pretreatment with the NO substrate L-arginine (300 mg/kg s.c.). Indomethacin (5 mg/kg i.v.) was ineffective in suppressing LPS-mediated gastroprotection. These results suggest that while Ca2+-dependent NO formation is inhibited by ethanol treatment, the inducible Ca2+-independent NO synthase plays a role in LPS-mediated gastroprotection against ethanol-mediated damage to the gastric mucosa.Key words: nitric oxide, lipopolysaccharide, ethanol, gastroprotection, dexamethasone.

Mo1265 Significance of atrophic Changes of Gastric Mucosa in Patients With Gastric Mucosal Injury in Low-Dose Aspirin Users

2016 ◽  
Vol 150 (4) ◽  
pp. S682-S683
Author(s):  
Yuji Shimada ◽  
Akihito Nagahara ◽  
Mariko Hojo ◽  
Daisuke Asaoka ◽  
Kentaro Izumi ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Low Dose ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
Dose Aspirin ◽  
Low Dose Aspirin
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