Anti-inflammatory and carbonic anhydrase restoring actions of yam powder (Dioscorea spp) contribute to the prevention of cysteamine-induced duodenal ulcer in a rat model.
ABSTRACT Increased acid output, accompanied with a defective defense system, is considered a fundamental pathogenesis of duodenal ulcer (DU). However, relapse of DU occurs despite proton pump inhibitors and H2 receptor antagonists, hence imposing the enforcement of the defense system. Dried powder of the yam tuber (Dioscorea spp) has been used in traditional folk medicine as a nutritional fortification. We hypothesized that dried-yam powder would prevent DU through improvement of anti-inflammatory actions and carbonic anhydrase (CA) activity. Therefore, we investigated the preventive effects of dried-yam powder against the cysteamine-induced DU and elucidated the underlying mechanisms. Duodenal ulcers were induced in Sprague-Dawley rats by intragastric administration of 500 mg/kg cysteamine-HCl. The dried-yam powder was used as a pretreatment before the cysteamine-HCl. The number and size of DU were measured. The expressions of inflammation mediators were checked in duodenal tissues, and the expressions of CAs and malondialdehyde levels were also examined. Cysteamine provoked perforated DU, whereas dried-yam powder significantly prevented DU as much as pantoprazole and significantly reduced the incidence of perforation. The messenger RNA expressions of cyclooxygenase-2 and inducible nitric oxide synthase were remarkably decreased in the yam group compared with the cysteamine group, and the serum levels of proinflammatory cytokines including interleukin-1β, interleukin-6, and tumor necrosis factor were significantly attenuated in the yam group. Cysteamine significantly decreased the expression of CAs, whereas yam treatment significantly preserved the expressions of CA IX, XII, and XIV. In conclusion, dried-yam powder exerts a significant protective effect against cysteamine-induced DU by lowering the activity of inflammatory cytokines and free radicals and restoring the activity of CAs, except in CA IV.
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ABSTRACT: Cysteamine and propionitrile, experimental duodenal ulcerogens, stimulated gastric acid secretion in the rat. Gastric acid secretion was measured by two separate methods, the conventional pylorus ligation technique and a non-invasive technique based on the pH dependent liberation of azure A from azuresin in the stomach with subsequent excretion of the liberated dye in the urine. Volume, acid concentration and acid content of gastric fluids aspirated immediately before the pylrous ligation were markedly increased 1,4 and 7 hours after a single dose of either cysteamine or propionitrile. Both acid concentration and acid output of gastric contents collected 30 minutes after pylorus ligation were also significantly elevated 1.5 hours after propionitrile and 4.5 hours after cysteamine. Significant increases in gastric acid secretion after these chemicals were also measured by the non-invasive technique which demonstrated a 4 to 6 fold increase in 24 hour urinary azure A output in rats injected with either propionitrile or cysteamine. Enhanced gastric acid output may play an important role in the pathogenesis of duodenal ulcer produced by propionitrile and cysteamine.Research communications in chemical pathology and pharmacology 03/1977; 16(2):311-23.
- American Journal Of Pathology 11/1978; 93(1):273-6. · 4.60 Impact Factor
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ABSTRACT: The mechanism and time for healing of cysteamine-induced duodenal ulcers in rats were investigated. Cysteamine induces a mixture of erosions, ulcers, and penetrating ulcers. These three stages of ulcerations healed in different ways and in different times. Erosions healed within three days by formation of new mucosa from the epithelium of the remaining parts of the crypts of Lieberkühn. The mucosa became completely normal within 15 days. Ulcers healed primarily by a contraction of the circular layer of the external muscle coat, thereby approaching the ulcer edges and reestablishing a complete layer of Brunner's glands in the submucosa. Healing was complete within 15 days. Penetrated ulcers healed very slowly by formation of new epithelium and Brunner's glands from the ulcer edges. The newly formed epithelium was desquamated unless protected by underlying Brunner's glands and the regeneration of these therefore determined the healing of the ulcer. Only a few of these ulcers had healed after 50 days. After 100 and 150 days, approximately 50% had healed, and after 200 days still only 64% had healed. Thus the cysteamine ulcer with destroyed muscle coat has a very prolonged healing and thereby represents a model for a chronic duodenal ulcer which may be of value as a model for testing treatments of duodenal ulcers.Digestive Diseases and Sciences 03/1985; 30(2):161-7. · 2.26 Impact Factor