Experimental Gastric Ulcers In Rats Research Articles

Gastroprotective activity of Cinnamomum tamala leaves on experimental gastric ulcers in rats

Cinnamomum tamala T. Nees & Eberm (Family Lauraceae) is used traditionally in Indian System of Medicine as carminative, anthelmintic, diuretic, and used in colic, dyspepsia, and diarrhea. This study was aimed to evaluate the gastroprotective effects of Cinnamomum tamala leaves. Cinnamomum tamala leaves extract (CTE; 50,100 and 200mg/kg body weight) was administered orally, twice daily for 5 days for prevention from ethanol (EtOH)-, cold-restraint stress (CRS)- and pylorus ligation (PL)-induced ulcers. Estimation of H(+)K(+)ATPase activity and gastric wall mucous were performed in EtOH-induced ulcer model, antioxidant enzyme activities was carried out in CRS-induced ulcer model, and various gastric secretion parameters like volume of gastric juice, acid output, and pH value were estimated in PL-induced ulcer model. A significant reduction in lesion index was observed in ulcer-induced animals treated with CTE at different doses when compared with ulcerated rats in all models. A significant decrease occurred in the level of H(+)K(+)ATPase, volume of gastric juice, and acid output. Simultaneously the level of gastric wall mucus and pH were increased significantly. These showed dose-dependent action of CTE. The antioxidant enzyme levels of LPO and SOD were decreased while administering CTE at different doses, compared with their control values. Contrary to this the level of CAT enzyme showed significant increase. The results of our study showed that Cinnamomum tamala possess significant gastroprotective activity, probably due to its free radical scavenging activity.

Anti-ulcer Activity of Curcumin on Experimental Gastric Ulcer in Rats and Its Effect on Oxidative Stress/Antioxidant, IL-6 and Enzyme Activities

To investigate the possible mechanism by which curcumin protects stomach during the acute chronic phase of gastric ulcer disease. The rats were divided into four groups and fasted for 2 days with free access to water. On the third day, the animals were fasted for a further 24 h with no access to water followed by surgery. Rats received different doses of curcumin (20, 40, and 80 mg/kg) or vehicle by oral gavage. Nineteen hours after ulcer induction, the rats were killed by decapitation. Stomach was opened along the greater curvature and ulcerative lesions were counted. Total juice acidity, neutrophils activity, mitochondrial activity, total antioxidants, paraoxonase (PON 1)/arylesterase and total peroxides were evaluated. DNA fragmentation (%) and pro-inflammatory cytokine IL-6 level were measured. The level of different gastro-cytoprotective effectors including total antioxidants and paraoxonase (PON 1)/arylesterase activities was measured. The anti-ulcer activity of curcumin was displayed by attenuating the different ulcerative effectors including gastric acid hyper-secretion, total peroxides, myeloperoxiase (MPO) activity, IL-6 and apoptotic incidence. Curcumin appears to have a propitious protective effect against gastric ulcer development.

Gastroprotective effect of standardized extract of Ficus glomerata fruit on experimental gastric ulcers in rats

Ethnopharmacological relevance Traditionally fruits of Ficus glomerata Roxb (Family: Moraceae) are used to treat anemia and gastrointestinal disorders. Aim Gastroprotective effect of 50% ethanolic extract of F. glomerata fruit (FGE) was studied in different gastric ulcer models in rats. Methods FGE (50, 100 and 200 mg/kg body weight) was administered orally, twice daily for 5 days for prevention from pylorus ligation (PL), ethanol (EtOH) and cold restraint stress (CRS) – induced ulcers. Estimation of H +K +ATPase activity and gastric wall mucous were performed in EtOH-induced ulcer and antioxidant enzyme activities in supernatant mitochondrial fraction of CRS-induced ulcers. Results FGE showed dose dependent inhibition of ulcer index in pylorus ligation, ethanol and cold restraint stress – induced ulcers. FGE prevents the oxidative damage of gastric mucosa by blocking lipid peroxidation and by significant decrease in superoxide dismutase, H +K +ATPase and increase in catalase activity. High performance thin layer chromatography (HPTLC) analysis showed the presence of 0.57% and 0.36% w/w of gallic acid and ellagic acid in FGE. Conclusions Our results show that F. glomerata possess significant gastroprotective activity which might be due to gastric defence factors and phenolics might be the main constituents responsible for this activity.

Effect of Brazilian green propolis on experimental gastric ulcers in rats

Propolis is a resinous hive product collected by honeybees from plants. The propolis produced in Southeastern of Brazil is known as green propolis because of its color. Modern herbalists recommend its use because it displays antibacterial, antifungal, antiviral, hepatoprotective, anti-inflammatory, immunomodulatory and anti-ulcer properties. The anti-ulcer activity of green propolis hydroalcoholic crude extract was evaluated by using models of acute gastric lesions induced by ethanol, indomethacin and stress in rats. Moreover, the effects of extract on gastric content volume, pH and total acidity, using pylorus ligated model were evaluated. Animals pretreated with propolis hydroalcoholic crude extract (50, 250 and 500 mg/kg) showed a significant reduction in lesion index, total affected area and percentage of lesion in comparison with control group ( p < 0.05) in the ethanol-induced ulcer model. Green propolis extract, at a higher dose (500 mg/kg), displayed a significant protection by reducing ( p < 0.05) the evaluated parameters in the gastric ulceration induced by indomethacin. In the stress-induced ulcer model it was observed a significant reduction ( p < 0.05) in those parameters in animals treated with green propolis extract (250 and 500 mg/kg). Regarding the pylorus ligated model it was observed that green propolis extract (250 and 500 mg/kg) displayed an anti-secretory activity, which lead to a reduction in the gastric juice volume, total acidity and pH. These findings indicate that Brazilian green propolis displays good anti-ulcer activity, corroborating the folk use of propolis preparations, and contributing for its pharmacological validation.

Effects of Danshen Decoction on experimental gastric ulcer in rats and mice

To investigate the preventive and therapeutic effects of Danshen Decoction on gastric ulcer in experimental animal models. The model of water immersion restraint stress ulcer in mice, and the models of acetic acid impaired gastric ulcer and pyloric ligation gastric ulcer in rats were established. The total gastric acid, the activity of pepsin and the amount of gastric wall binding mucus were detected. Danshen Decoction reduced the acute gastric mucosal lesion. The effect of 5.0 or 10.0 g/kg group was obviously better than that of the normal saline control group (P<0.05 and P<0.01 respectively). Danshen Decoction accelerated the healing of ulcer induced by acetic acid significantly, and increased the content of gastric wall binding mucus (P<0.01); and it also inhibited the formation of gastric ulcer induced by pyloric ligation, while having no influence on the secretion of gastric acid and the activity of pepsin. Danshen Decoction has a significant anti-ulcerative effect, which may be related to improving the gastric mucosal defensive function.

Experimental gastric ulcer: gastro- and duodenoprotective effects of sibusol.

We studied the influence of pretreatment with chemical mildronate analogue sibusol on the course of experimental gastric ulcer in rats. Sibusol produced a protective effects on the stomach and duodenum.

Effects of sea buckthorn ( Hippophaë rhamnoides L.) seed and pulp oils on experimental models of gastric ulcer in rats

Oils from sea buckthorn ( Hippophaë rhamnoides L.) seeds and berries have traditionally been used in the treatment of disorders of skin and mucosa in China. Compared with the negative control, oral administration of CO 2-extracted seed and pulp oils, 7.0 ml · kg −1 · day −1 significantly reduced ulcer formation in water-immersion ( P<0.05) and reserpine-induced ( P<0.01) models in rats. In addition, administration of the two oils, 3.5 ml · kg −1· day −1, significantly reduced the index of pylorus ligation-induced gastric ulcer ( P<0.05) and sped up the healing process of acetic acid-induced gastric ulcer ( P<0.01). The results suggested that the CO 2-extracted sea buckthorn seed and pulp oils have both preventive and curative effects against experimental gastric ulcers in rats.

Role of epidermal growth factor, interleukin-1 and lipid peroxidation in healing of experimental gastric ulcer in rats

The aim of our study was to evaluate the role of the epidermal growth factor (EGF), interleukin-1 (IL-1) and of lipid peroxides (TBARS) in the development and healing of experimental gastric ulcer in the rat. In 66 male Sprague Dowley rats, gastric ulcer was induced by means of the serosal application of 100% acetic acid. The animals were followed up for 1 (6 cases), 3 (6) and 5 (6) hours, and 1 (6 cases), 2 (6), 3 (7), 5 (6), 10 (6) 15 (6) and 21 (6) days. Five animals were sham operated. Samples from the ulcer margin (U), from an ulcer adjacent area (UAA) and from the antrum (A) were obtained. All treated animals developed gastric ulcer, evident just after one hour; the ulcer progressively healed and after 21 days all were scarred. Mucosal U-EGF significantly increased immediately after ulcer induction; it progressively and slowly decreased paralleling ulcer scarring. UAA-EGF and A-EGF behaved likewise: they significantly increased after 1, 3 and 5 hours and returned to normal levels just 1 day after ulcer induction. Variations in mucosal IL-1 were similar to those in EGF, a correlation being found between these two parameters. The EGF serum levels of rats with ulcers of 1 and 5 hours, were significantly lower than those of controls. One day after ulcer induction, U-TBARS levels were increased, and the high levels persisted, even when the ulcers had healed. In conclusion: (1) the rapid increase in mucosal EGF occurring in the presence of gastric ulcer may be consequent to an enhanced local and/or submandibular production; (2) the parallel behaviour between EGF and IL-1 suggests that this cytokine may play a role in stimulating EGF production; (3) chronic gastric ulcer is associated with an enhancement of lipid peroxidation phenomena, which persist after healing and which may create a “loci minoris resistentiae”.

Tobacco cigarette smoke aggravates gastric ulcer in rats by attenuation of ulcer margin hyperemia

We tested the hypothesis that attenuation of the hyperemia at the margin of acetic acid-induced gastric ulcer in rats by tobacco cigarette smoke will increase the size of the ulcer in the acute and the healing stages. Compared with the adjacent mucosa, blood flow measured by hydrogen gas clearance at the ulcer margin was significantly higher (ulcer margin hyperemia). Tobacco cigarette smoke and subcutaneous nicotine but not nicotine-free smoke from non-tobacco cigarettes significantly attenuated the ulcer margin hyperemia in a dose-related fashion. Repeated exposure of the rats to tobacco cigarette smoke increases ulcer size in the acute and the healing stages. Subcutaneous nicotine but not nicotine-free smoke also increased the size of ulcers in the acute stage. These results indicate that the nicotine in tobacco cigarette smoke may be responsible in part for its adverse effects. We conclude that attenuation of the hyperemia at the ulcer margin is a plausible explanation for the mechanism of the adverse effect of the tobacco cigarette smoke on experimental gastric ulcers in rats.

P-353 - Anti-ulcer effects of ME3407 on experimental gastric ulcers in rats.

P-353 - Anti-ulcer effects of ME3407 on experimental gastric ulcers in rats.

Influence of capsaicin-sensitive afferent fibers on acetic acid-induced chronic gastric ulcers in rats.

Accumulating evidence indicates that capsaicin-sensitive afferent fibers play a pivotal role in acute gastroprotection. However, whether they also influence healing of chronic gastric ulcers is still unknown. The effects of ablation of sensory neurons on acetic acid-induced chronic gastric ulcers in rats were investigated at morphologic and biochemical levels by computerized imaging analysis of the ulcerated area, histologic examination, and neuropeptide determination. Afferent nerve ablation, as a result of treating rats with a neurotoxic dose of capsaicin (50 + 50 mg/kg subcutaneously over 2 days), produced a significant increase in the ulcer area at 1 and 2 weeks after acetic acid injection. The delay in ulcer healing was associated with a marked and persistent decrease in tissue calcitonin gene-related peptide-like immunoreactivity, whereas gastric vasoactive intestinal polypeptide was unaffected by capsaicin pretreatment. Histologically, as compared with control rats, capsaicin-desensitized animals only differed in a slight increase in the inflammatory infiltrate during the early phase of ulcer formation. These findings suggest that capsaicin-sensitive afferent fibers may play a role in the healing of chronic experimental gastric ulcers in rats, but the underlying mechanisms remain to be elucidated and deserve further investigation.

Solcoseryl: Ulcerostatic effect and its possible mechanisms

It is shown that the level of DNA, RNA, collagen, non-collagen proteins, hexoses and glycosaminoglycans is changed when making the experimental gastric ulcer in rats. Solcoseryl stabilises the level of DNA, RNA and collagen, stimulating the reparation processes in ulcer.

P-51 - Anti-ulcer effect of IO-21 on various experimental gastric ulcers in rats.

P-51 - Anti-ulcer effect of IO-21 on various experimental gastric ulcers in rats.

Effects of Prostaglandins on Hydrocortisone-Induced Delayed Healing of Chronic Gastric Ulcers in the Rat

We have previously shown that chronic steroid administration delays the healing of experimental gastric ulcers in rats. This study was designed to test the beneficial effects of 16,16-dimethylprostaglandin E2 or TRY-200, a stable prostaglandin I2 analogue, on the delayed healing by hydrocortisone (HC) of chronic gastric ulcers in rats. Chronic gastric ulcers were produced in male Wistar rats, weighing 180 g, by serosal application of 100% acetic acid. The rats were randomly divided into six groups: (1) saline, (2) saline, HC-treated, (3) 10 micrograms/kg of 16,16-dimethylprostaglandin E2, (4) TRY-200, a stable prostaglandin I2 analogue, at 5 micrograms/kg, or (5) 10 micrograms/kg, or (6) 30 micrograms/kg. All rats, except for control, were given daily intraperitoneal injection of 2.5 mg/kg of HC sodium phosphate. Tested drugs were administered intragastrically twice a day for 2 weeks. Rats were killed 14 days later and ulcer size was measured. Chronic administration of HC sodium phosphate resulted in a significant delay of ulcer healing induced by acetic acid. Treatment with TRY-200 at 10 or 30 micrograms/kg abolished the deleterious effect of steroids, whereas 16,16-dimethylprostaglandin E2 had no effect. These results indicate that prostaglandin I2 is more effective than prostaglandin E2 in reversing the delayed healing by steroids of chronic gastric ulcers in the rat.

Effects of sucralfate, lansoprazole, and cimetidine on the delayed healing by hydrocortisone sodium phosphate of chronic gastric ulcers in the rat

We have previously shown that chronic sucralfate ingestion stimulates gastric epithelial proliferation in rats, which may explain one of the beneficial effects of sucralfate in healing of peptic ulcers. In a separate study, we have found that chronic steroid administration delays the healing of experimental gastric ulcers in rats. This study was designed to test the beneficial effects of sucralfate, cimetidine, and lansoprazole (AG-1749, a new proton pump inhibitor), on the delayed healing by steroids in rat chronic gastric ulcers. Chronic gastric ulcers were produced in male Wistar rats, weighing 180 g, by the application of 100% acetic acid. The rats were randomly divided into five groups; (1) control, (2) vehicle alone, (3) 10 mg/kg lansoprazole, (4) 500 mg/kg sucralfate, and (5) 100 mg/kg cimetidine. Except for controls, all rats received daily intraperitoneal injections of 2.5 mg/kg hydrocortisone sodium phosphate. Tested drugs were administered intragastrically (lansoprazole and sucralfate) or intraperitoneally (cimetidine) twice a day for 2 weeks. Rats were sacrificed 14 days later and ulcer size was measured. Chronic administration of hydrocortisone sodium phosphate resulted in a significant delay of ulcer healing induced by acetic acid. Treatment with either lansoprazole or sucralfate abolished the deleterious effect of steroids, whereas cimetidine had no effect. These results indicate that lansoprazole and sucralfate overcome the delayed healing by steroids of chronic gastric ulcers in the rat.

Central nervous system action of calcitonin to alter experimental gastric ulcers in rats

The central nervous system action of calcitonin to influence various experimental models of gastric ulcers and gastric function was studied in rats fasted for 24 h. Intracisternal injection of salmon calcitonin (5 μg) completely suppressed gastric ulcerations induced by exposure to cold restraint stress, intracisternal injection of a stable thyrotropin-releasing hormone analogue, or peroral administration of aspirin. By contrast, intracisternal calcitonin enhanced gastric lesions elicited by peroral administration of 40% ethanol or 0.6 N HCl. Calcitonin action was dose-dependent (0.01–1 μg) and central nervous system mediated inasmuch as intravenous calcitonin, given at a dose 50-fold higher than that effective intracisternally, did not significantly modify gastric mucosal injuries elicited by aspirin or ethanol. Intracisternal injection of calcitonin at 0.01 μg inhibited gastric acid output by 90% in pylorus-ligated rats and suppressed gastric emptying of a liquid meal by 63%–94% in doses ranging from 0.01 to 5 μg. Prostaglandin generation in the gastric mucosa was not modified by intracisternal injection of calcitonin. These results demonstrate that intracisternal calcitonin acts within the brain to potently prevent ulcer formation elicited by stress, thyrotropin-releasing hormone analogue, or aspirin, but is not cytoprotective against necrotizing agents. Calcitonin action is not related to modification of gastric prostaglandin generation but it may involve the inhibition of gastric secretory and motor function.

Production, Isolation and Pharmacological Studies of AI-77s

Two potent gastroprotective substances against experimental gastric ulcers in rats induced by stress and five of their analogues were isolated from the culture broth of bacterial strain AI-77 which was classified taxonomically as Bacillus pumilus. Physico-chemical properties and pharmacological activities of the seven compounds were examined and compared with each other.

Studies on AI-77s, microbial products with pharmacological activities. Part I. Production, isolation and pharmacological studies of AI-77s.

Two potent gastroprotective substances against experimental gastric ulcers in rats induced by stress and five of their analogues were isolated from the culture broth of bacterial strain AI-77 which was classified taxonomically as Bacillus pumilus. Physico-chemical properties and pharmacological activities of the seven compounds were examined and compared with each other.

Study of antiulcer activity of aqueous extract of leaves of Pyrenacantha staudtii (family icacinaceae) using various models of experimental gastric ulcer in rats

The antiulcer activity of an aqueous extract of Pyrebnacantha staudtii was studied in rats and was compared with that of cimetidine. Ulcers were induced in rats by means of various experimental models: aspirin, indomethacin, serotonin and reserpine. The extract was found to have significant antiulcer activity against all the models studied. Cimetidine was found to be ineffective agianst serotonin- and reserpine-induced ulcers.

Experimental Gastric Ulcer in Rats and Mice as a Psychosomatic Disease Model(Animal models in psychosomatic disorders)

Experimental Gastric Ulcer in Rats and Mice as a Psychosomatic Disease Model(Animal models in psychosomatic disorders)