beta-carotene and Stomach-Ulcer

The peptic ulcer of stomach and duodenum are the more often occuring complications of steroid treatment in children with chronic glomerulonephrite. Dinamic investigation has shown that the using of beta-carotin oily solution in therapy of this complications increases the efficiency of traditional treatment. It has been shown that beta-carotene administration speeds the reparation of stomach and duodenum ulcers, saves adequate serum concentration of beta-carotene and retinol. The data obtained demonstrate that beta-carotene administration in the complex therapy of chronic glomerulonephrite patient with gastroenteropathy should be recommended.

Topics: Administration, Oral; Adolescent; Anti-Inflammatory Agents; Antioxidants; beta Carotene; Child; Child, Preschool; Chronic Disease; Diet, Protein-Restricted; Duodenal Ulcer; Endoscopy; Gastric Mucosa; Glomerulonephritis; Humans; Prednisolone; Stomach Ulcer

Carotenoids and retinoids have been reported to reduce gastrointestinal mucosa damage from a variety of irritants. We performed double-blind, placebo-controlled endoscopic trial to evaluate the effect of chronic beta-carotene supplementation upon the gastric mucosal response to acute aspirin injury. Six subjects taking chronic beta-carotene and six taking placebo each ingested 650 mg of aspirin after an endoscopy confirmed normal gastric mucosa. Three hours later, mucosal lesions were counted at repeat endoscopy. beta-Carotene did not prevent acute mucosal injury better than placebo.

Topics: Acute Disease; Aged; Aspirin; beta Carotene; Carotenoids; Double-Blind Method; Female; Gastric Mucosa; Gastroscopy; Humans; Male; Middle Aged; Prospective Studies; Stomach Ulcer

Decoctions or infusions of the stem bark of Byrsonima japurensis A. Juss. (Malpighiaceae) are widely used as an anti-inflammatory drug in folk medicine of Amazonas State (Brazil).. To evaluate the pharmacological potential of an aqueous extract of the stem bark of Byrsonima japurensis (BJEA) to scientifically verify of its traditional use.. Anti-inflammatory, antihyperalgesic and antiulcer activities were evaluated in Wistar rats, a Hippocratic screening was performed in Swiss mice to evaluate the toxic effects, and antiplatelet evaluation was performed in human platelet rich plasma assay. Additionally, antioxidant activity was evaluated by superoxide radical scavenging method and β-carotene bleaching test.. Anti-inflammatory, antihyperalgesic and gastroprotective activities were observed in rats treated orally with different doses of BJEA. While signals of toxicity were observed in the mice treated with a very high dose of extract (5000mg/kg), no death occurred. BJEA also showed expressive antiplatelet and antioxidant activities in vitro.. According to our results, it was concluded that stem bark of Byrsonima japurensis has significant and safe anti-inflammatory activity, which is closely related with their potent antioxidant activity, supporting the folk medicinal use of this species.

Topics: Analgesics; Animals; Anti-Inflammatory Agents; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Antioxidants; beta Carotene; Brazil; Carrageenan; Edema; Female; Humans; Male; Malpighiaceae; Mice; Mice, Inbred BALB C; Pain; Phytotherapy; Plant Bark; Plant Extracts; Plant Stems; Platelet Aggregation Inhibitors; Rats; Rats, Wistar; Stomach Ulcer; Superoxides

The antiulcerogenic and antioxidant properties of Matricaria chamomilla L. (Compositae) hydroalcoholic extract (MCE) on ethanol-induced gastric mucosal injury were investigated in rats. After the induction of gastric mucosal injury, all groups were sacrificed; the gastric ulcer index was calculated, and malondialdehyde (MDA) and reduced glutathione (GSH) in whole blood and gastric tissue, and serum ascorbic acid, retinol, and beta-carotene levels were measured in all groups. Pretreatment with MCE at some doses significantly reduced gastric lesions. Again, some doses of MCE significantly reduced the MDA, and significantly increased GSH levels in gastric tissue or whole blood. Serum beta-carotene and retinol levels were significantly higher in the 200 mg/kg MCE-administered group with respect to control. As a result, MCE clearly has a protective effect against ethanol-induced gastric mucosal lesions, and this effect, at least in part, depends upon the reduction in lipid peroxidation and augmentation in antioxidant activity.

Topics: Animals; Anti-Ulcer Agents; Antioxidants; Ascorbic Acid; beta Carotene; Drug Evaluation, Preclinical; Ethanol; Glutathione; Lipid Peroxidation; Male; Malondialdehyde; Matricaria; Phytotherapy; Plant Extracts; Rats; Rats, Wistar; Stomach Ulcer; Vitamin A

Reactive oxygen species (ROS) play critical roles in Helicobacter pylori (H. pylori)-associated gastric ulceration and carcinogenesis. Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are involved in H. pylori-induced gastric diseases. Previously we demonstrated that H. pylori in Korean isolates induced the activation of mitogen-activated protein kinases (MAPK) and oxidant-sensitive transcription factors NF-kappaB and AP-1 which mediates the expression of iNOS and COX-2 in gastric epithelial AGS cells. beta-Carotene shows antioxidant activity and inhibits NF-kappaB-dependent gene expression in various cells. Present study aims to investigate whether beta-carotene inhibits H. pylori-induced expression of iNOS and COX-2 by suppressing the activation of MAPK, NF-kappaB, and AP-1 in gastric epithelial AGS cells. HP99 (H. pylori in Korean isolates) was added to AGS cells at the ratio of bacterium/cell, 300/1. beta-carotene inhibited H. pylori-induced increase in ROS level, the activation of MAPK (p38, the c-Jun NH2-terminal protein kinases, the extracellular signal-regulated kinases), NF-kappaB, and AP-1 and the expression of iNOS and COX-2 in AGS cells.. beta-carotene inhibits oxidant-mediated activation of inflammatory signaling and suppresses the expression of iNOS and COX-2 in gastric epithelial AGS cells infected with H. pylori.

Topics: beta Carotene; Cell Line; Cyclooxygenase 2; DNA-Binding Proteins; Enzyme Activation; Epithelial Cells; Extracellular Signal-Regulated MAP Kinases; Gastric Mucosa; Gene Expression Regulation, Enzymologic; Helicobacter Infections; Helicobacter pylori; Humans; I-kappa B Kinase; Inflammation Mediators; JNK Mitogen-Activated Protein Kinases; NF-kappa B; Nitric Oxide Synthase Type II; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Reactive Oxygen Species; RNA, Messenger; Stomach Ulcer; Transcription Factor AP-1

Frequently used for humans as non-steroidal anti-inflammatory drug, naproxen has been known to induce ulcerative gastric lesion. The present study investigated the in vivo protective effect of astaxanthin isolated from Xanthophyllomyces dendrorhous against naproxen-induced gastric antral ulceration in rats. The oral administration of astaxanthin (1, 5, and 25 mg/kg of body weight) showed a significant protection against naproxen (80 mg/kg of body weight)-induced gastric antral ulcer and inhibited elevation of the lipid peroxide level in gastric mucosa. In addition, pretreatment of astaxanthin resulted in a significant increase in the activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. A histologic examination clearly proved that the acute gastric mucosal lesion induced by naproxen nearly disappeared after the pretreatment of astaxanthin. These results suggest that astaxanthin removes the lipid peroxides and free radicals induced by naproxen, and it may offer potential remedy of gastric ulceration.

Topics: Adjuvants, Immunologic; Animals; beta Carotene; Disease Models, Animal; Dose-Response Relationship, Drug; Glutathione Peroxidase; Male; Malondialdehyde; Naproxen; Pyloric Antrum; Rats; Rats, Sprague-Dawley; Stomach Ulcer; Superoxide Dismutase; Time Factors; Xanthophylls

Ethanol has been found to induce ulcerative gastric lesion in humans. The present study investigated the in vivo protective effect of astaxanthin isolated from the Xanthophyllomyces dendrorhous mutant against ethanol-induced gastric mucosal injury in rats. The rats were treated with 80% ethanol for 3 d after pretreatment with two doses of astaxanthin (5 and 25 mg/kg of body weight respectively) for 3 d, while the control rats received only 80% ethanol for 3 d. The oral administration of astaxanthin (5 and 25 mg/kg of body weight) showed significant protection against ethanol-induced gastric lesion and inhibited elevation of the lipid peroxide level in gastric mucosa. In addition, pretreatment with astaxanthin resulted in a significant increase in the activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. A histologic examination clearly indicated that the acute gastric mucosal lesion induced by ethanol nearly disappeared after pretreatment with astaxanthin.

Topics: Animals; Basidiomycota; beta Carotene; Catalase; Dose-Response Relationship, Drug; Ethanol; Gastric Mucosa; Glutathione Peroxidase; Male; Malondialdehyde; Models, Biological; Mutation; Rats; Rats, Sprague-Dawley; Severity of Illness Index; Stomach Ulcer; Superoxide Dismutase; Xanthophylls

Astaxanthin (Asx), one of the carotenoids, is a red pigment in fish and Crustaceans, and possesses stronger reduction properties than conventional carotenoids, like beta-carotene. However, little is known about the biochemical properties and physiological functions of astaxanthin. The effects of astaxanthin and vitamin C on stressed rats were studied physiologically and biochemically. beta-Carotene and three kinds of astaxanthins, which were extracted from Haematococcus and Phaffia, and synthesized chemically, were used in these experiments. These rats given astaxanthins or beta-carotene had stress induced on the 12th day by immersing the rats in chest-level water at 20 degrees C for 24 h after fasting for 24 h. Rats given astaxanthins or beta-carotene prior to stressing were appreciably protected against the evolution of gastric ulcerations in relation to control rats. Ulcer indexes in particular were smaller with the rat group fed astaxanthin extracted from Haematococcus than the other groups. Next, the effects of Asx and/or vitamin C on the protection of evolution of gastric ulcer in stressed rats were persued by the same methods as described above. The results showed that rats given Asx or vitamin C were appreciably protected against the evolution of gastric ulcerations in relation to control rats. The effects were more intense, especially in rats simultaneously supplied Asx and vitamin C than in rats taking either Asx or vitamin C. It was suggested that the simultaneous supplementation of food substances with astaxanthin and vitamin C would supply enough antioxidants to offset stress-related injuries.

Topics: Alanine Transaminase; Animals; Antioxidants; Ascorbic Acid; Aspartate Aminotransferases; beta Carotene; Diet; gamma-Glutamyltransferase; Immersion; Male; Rats; Rats, Wistar; Stomach Ulcer; Stress, Physiological; Triglycerides; Xanthophylls

It was shown that in patients with hypertension, duodenal and gastric ulcers and erosive gastritis leukopenia and lymphopenia are seen. At the same time contents of T- and B-lymphocytes are decreased and contents of C- lymphocytes are increased in circulation blood. Peroral daily intake of 20 mg of beta-carotene during 3-4 weeks caused increasing the contents of B- and T-cells and decreasing contents of C-lymphocytes in blood of patients.

Topics: Adjuvants, Immunologic; Administration, Oral; B-Lymphocytes; beta Carotene; Carotenoids; Duodenal Ulcer; Gastritis; Humans; Hypertension; Lymphocyte Count; Peptic Ulcer; Stomach Ulcer; T-Lymphocytes; Time Factors

As to earlier observations that beta-carotene prevents the development of gastric mucosal injury produced by different noxious agent, however, its cytoprotective effect can be abolished by acute surgical vagotomy. The aim of this study was to evaluate the possible correlation between the gastric mucosal cytoprotective effect of beta-carotene and its gastric mucosal level in rats treated with IND. The gastric mucosal damage was produced by the administration of IND (20 mg/kg s.c.). The instillation of beta-carotene and acute surgical vagotomy (ASV) or SHAM operation were carried out 30 min before IND treatment. The rats were sacrificed 4 h after IND application, and the number and severity of gastric mucosal erosions were noted. The blood rats was collected quantitatively, the liver and the gastric mucosa were removed, and the beta-carotene and vitamin A level of the gastric mucosa, serum and liver were measured with HPLC. It was found that: 1. Beta-carotene induced gastric cytoprotection in SHAM-operated rats treated with IND but its effect disappeared after ASV. 2. Although the beta-carotene level of the gastric mucosa increased its concentration was not elevated in the serum of intact and vagotomized animals either. 3. Vitamin A Formation was not detected in the liver of animals with or without ASV. It was concluded that the lack of intake of beta-carotene into the gastric mucosa can not play etiologic role in the failure of gastric cytoprotection of rats with acute bilateral surgical vagotomy.

Topics: Animals; beta Carotene; Carotenoids; Chromatography, High Pressure Liquid; Female; Gastric Mucosa; Indomethacin; Liver; Male; Rats; Rats, Sprague-Dawley; Spectrophotometry, Ultraviolet; Stomach Ulcer; Vagotomy

Topics: Animals; Anti-Ulcer Agents; beta Carotene; Carotenoids; Gastric Mucosa; Hydrochloric Acid; Male; Rats; Rats, Inbred Strains; Stomach Ulcer

It was earlier known that PGI2 and beta-carotene have a cytoprotective effect, but the similarities and the differences of their mechanisms were not clear. The gastric mucosal lesions were produced by ig. administration of 1 ml 96% ethanol and 1 ml 0.6 N HCl in rats. The 5 and 50 micrograms/kg dose of PGI2 and the 1 and 10 mg dose of beta-carotene was given 30 min. earlier. The animals were sacrified 1, 5, 15, 30 and 60 minutes after the administration of the necrotizing agent. The number and the severity of gastric mucosal lesions were noted. It was found that the number and the severity of gastric ulcers were dose-dependently decreased in each model after using either PGI2 or beta-carotene. The inhibiting effect of PGI2 appeared in the first last 15 minutes while beta-carotene was effective from 15 to 60 minutes.. The mechanism of the cytoprotection induced by PGI2 differ from the beta-carotene induced one. PGI2 plays a part in the earlier vascular phase. beta-carotene modulates the repair mechanisms.

Topics: Animals; beta Carotene; Carotenoids; Epoprostenol; Ethanol; Female; Gastric Mucosa; Hydrochloric Acid; Male; Rats; Rats, Inbred Strains; Stomach Ulcer; Time Factors

The aim of the study was to evaluate the influence of atropine, PGF2 alpha and cimetidine on the gastric cytoprotective effect of beta-carotene. Mucosal damage was produced by intragastric (i.g.) addition of 96% ethanol in CFY-strain rats of both sexes weighing 180-220 g. Gastric cytoprotection caused by i. g. pretreatment with 1.0 mg/kg beta-carotene 30 minutes before ethanol administration, was observed after 1 hour. Atropine (0.5 mg/kg), cimetidine (50 mg/kg) and PGF2 alpha (200 micrograms/kg) were given intraperitoneally (i.p.) 30 minutes before ethanol administration with and without beta-carotene and the changes in the number and severity of the gastric ulcers were detected. PGF2 alpha did not influence the gastric cytoprotective effect of beta-carotene meanwhile it was inhibited by atropine and markedly by cimetidine. Deleterious effect of cimetidine on the beta-carotene-induced cytoprotection may be explained perhaps by the adverse effect of the two compounds on ATP-cAMP transformation hereby counteracting one another, but more data are needed to the better understanding of drug interactions relating to mucosal cytoprotection.

Topics: Animals; Atropine; beta Carotene; Carotenoids; Cimetidine; Dinoprost; Ethanol; Female; Gastric Mucosa; Male; Rats; Rats, Inbred Strains; Stomach Ulcer

The aims of our experiments were to clear up the possible correlations between the free radical mechanisms and the gastric cytoprotection of beta-carotene on HCl-induced gastric mucosal lesions. The beta-carotene was intragastrically given in doses of 1 and 10 mg/kg and 30 min. later 1 ml 0.6 N HCl was given to provoke the mucosal damage. After 1, 5, 15, 30 and 60 min. the animals were sacrificed. The number and severity of gastric mucosal lesions were calculated. The superoxide dismutase (SOD), glutathion peroxidase (GPX), catalase (CAT) activity and the malondialdehyde (MDA) and reduced glutathion (GSH) contents were determined from the gastric mucosa of rats. It was found that 1. beta-carotene was able to reduce the number and severity of ulcers only after 30 min.; 2. the CAT activity was decreased at 60 min. by carotene; 3. the GPX activity became dissimilar in the different groups after 15 min; 4. the changes of GSH were found to be similar ones; 5. the SOD activity was lower during the cyto-protection; 6. the MDA level remained practically unchanged. It has been concluded that 1. the free radicals are the consequences of the development of gastric ulcer and cytoprotection; 2. the scavenger character of beta-carotene is involved in its cytoprotective effect.

Topics: Animals; beta Carotene; Carotenoids; Catalase; Disease Models, Animal; Female; Free Radicals; Gastric Mucosa; Glutathione; Glutathione Peroxidase; Hydrochloric Acid; Male; Malondialdehyde; Oxygen; Rats; Rats, Inbred Strains; Stomach Ulcer; Superoxide Dismutase

The effects of different doses (0.01-0.1-1.0-10.0/mg/kg-1) of beta-carotene were studied on gastric secretory responses of 4 hr pylorus-ligated rats: development of gastric mucosal damage (as assessed by number and severity of lesions) produced by intragastric administration of 0.6 M HCl; tissue level of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), adenylate pool (ATP + ADP + AMP), ratio of ATP X ADP-1, "energy charge" (ATP + 0.5 ADP X X (ATP + ADP + AMP)-1) (during the development of gastric mucosal damage by 0.6 M HCl and of gastric cytoprotection by beta-carotene. It was found that beta-carotene did not decrease the gastric secretory responses of 4 hr pylorus-ligated rats; The development of gastric mucosal damage could be decreased dose-dependently by the administration of beta-carotene; the ATP transformation could be decreased by beta-carotene; the tissue levels of cAMP and AMP could be increased significantly and dose-dependently by beta-carotene; the ratio of ATP X ADP-1 could be increased significantly and dose-dependently by beta-carotene; the values of adenylate pool and "energy charge" remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adenosine Triphosphate; Animals; beta Carotene; Carotenoids; Cell Membrane; Cyclic AMP; Dose-Response Relationship, Drug; Energy Metabolism; Female; Gastric Acid; Gastric Mucosa; Hydrochloric Acid; Male; Rats; Stomach Ulcer

Gastric mucosal damage was produced in rats by the intragastric administration of 96% ethanol or 0.6 M HCl, according to the method of Robert et al. Vitamin A or beta-carotene, in doses of 10 mg/kg, given intragastrically 30 min before the administration of the necrotizing agents. The animals were killed 1 hr after the administration of the necrotizing agents. The following experimental parameters were studied, without and with application of vitamin A and beta-carotene; number of gastric lesions (ulcers); severity of gastric mucosal lesions (ulcers); gastric mucosal superoxide dismutase (SOD) activity. It was found that; vitamin A and beta-carotene, in doses of 10 mg/kg, are able to prevent significantly both the number and severity of gastric mucosal lesions (ulcers) produced by the application of 96% ethanol or 0.6 M HCl; the significant increase of ethanol-induced gastric mucosal SOD activity can be inhibited by the application of vitamin A and beta-carotene; vitamin A and beta-carotene are capable of preventing the development of gastric mucosal lesions (ulcers) produced by the intragastric administration of 0.6 M HCl, while these agents fail to compensate for the HCl-induced decrease of gastric mucosal SOD activity. It has been suggested that; vitamin A and beta-carotene are gastric cytoprotective agents; the ulcer preventive effects of vitamin A and beta-carotene are partly dependent on their scavanger behaviour.

Topics: Animals; beta Carotene; Carotenoids; Female; Gastric Mucosa; Male; Rats; Stomach Ulcer; Superoxide Dismutase; Vitamin A