astaxanthine and Stomach-Ulcer

The purpose of this study was to investigate the effect of astaxanthin extracted from Paracoccus carotinifaciens on gastric mucosal damage in murine gastric ulcer models. Mice were pretreated with astaxanthin for 1 h before ulcer induction. Gastric ulcers were induced in mice by oral administration of hydrochloride (HCl)/ethanol or acidified aspirin. The effect of astaxanthin on lipid peroxidation in murine stomach homogenates was also evaluated by measuring the level of thiobarbituric acid reactive substance (TBARS). The free radical scavenging activities of astaxanthin were also measured by electron spin resonance (ESR) measurements. Astaxanthin significantly decreased the extent of HCl/ethanol- and acidified aspirin-induced gastric ulcers. Astaxanthin also decreased the level of TBARS. The ESR measurement showed that astaxanthin had radical scavenging activities against the 1,1-diphenyl-2-picrylhydrazyl radical and the superoxide anion radical. These results suggest that astaxanthin has antioxidant properties and exerts a protective effect against ulcer formation in murine models.

Topics: Acids; Animals; Anti-Ulcer Agents; Aspirin; Biphenyl Compounds; Disease Models, Animal; Ethanol; Free Radical Scavengers; Gastric Mucosa; Lipid Peroxidation; Male; Mice; Paracoccus; Picrates; Stomach; Stomach Ulcer; Thiobarbituric Acid Reactive Substances; Xanthophylls

This study is to investigate therapeutic effect of astaxanthin on acetic acid-induced gastric ulcer in rats. Rats were divided into control group, ulcer control group, and astaxanthin (5, 10, and 25 mg x kg(-1)) groups at random, 8 rats in each group. After administered for 10 days consecutively, all the rats were sacrificed. The area of ulcer and the levels of MDA, SOD, CAT and GSH-Px in gastric mucosa were measured. Compared with ulcer control group, in astaxanthin (5, 10, and 25 mg x kg(-1)) groups, the area of ulcer was decreased significantly. Level of MDA decreased while activities of SOD, CAT and GSH-Px increased (P < 0.05). Astaxanthin has good therapeutic effect on acetic acid-induced gastric ulcer in rats. Eliminating free radical and improving local blood circulation of the ulcer may be the mechanism of action.

Topics: Acetic Acid; Animals; Anti-Ulcer Agents; Antioxidants; Catalase; Gastric Mucosa; Glutathione Peroxidase; Male; Malondialdehyde; Random Allocation; Rats; Rats, Sprague-Dawley; Stomach Ulcer; Superoxide Dismutase; Xanthophylls

The anti-ulcer properties of astaxanthin fractions such as total carotenoid and astaxanthin esters from Haematococcus pluvialis were evaluated in ethanol-induced gastric ulcers in rats. Since oxygen radical release is a pathogenic factor of ethanol-induced gastric damage, astaxanthin - a free radical scavenger, was investigated as a potential ulcer preventive agent. Astaxanthin fractions - total carotenoid and astaxanthin esters were orally administered to experimental rats at 100, 250 and 500 microg/kg b.w. prior to ulcer induction. Alcian blue binding assay indicates that, total carotenoid and astaxanthin esters at 500 microg/kg b.w could protect gastric mucin approximately 40% and 67% respectively. Pre-treatment with astaxanthin esters, also resulted in significant increase in antioxidant enzyme levels - catalase, superoxide dismutase, and glutathione peroxidase in stomach homogenate. Histopathological examination substantiated the protective effect of astaxanthin in pre-treated rats. The increased antioxidant potencies such as free radical scavenging activity with an IC(50) of approximately 8 microg/ml and reducing power abilities (59 x 10(3) U/g) in vitro, reveal that H. pluvialis astaxanthin may protect gastric mucosal injury by antioxidative mechanism. In addition, approximately 23 fold increased lipoxygenase-inhibitory property, in comparison with standard astaxanthin and significant H(+), K(+)-ATPase-inhibitory activity of astaxanthin esters, in comparison with known proton pump blocking anti-ulcer drug - omeprazole, may envisage the potential gastroprotective effect by regulating the gastric mucosal injury and gastric acid secretion by the gastric cell during ulcer disease.

Topics: Animals; Anti-Ulcer Agents; Antioxidants; Carotenoids; Chlorophyta; Female; Gastric Mucosa; Lipid Peroxidation; Lipoxygenase Inhibitors; Male; Proton Pump Inhibitors; Rats; Rats, Wistar; Stomach Ulcer; Xanthophylls

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