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
CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, Korea.Nutrition research (Impact Factor: 2.47). 08/2013; 33(8):677-85. DOI: 10.1016/j.nutres.2013.05.019
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.
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ABSTRACT: The effects of fluid percussion trauma on brain interleukin (IL)-6, IL-1 and tumor necrosis factor-alpha (TNF-alpha) levels have been studied. In the cortex and hippocampus of control and sham-operated rats, the levels of these cytokines were very low (below 4 units/mg protein) and constant. IL-6 and IL-1 levels in the ipsilateral cortex increased rapidly following trauma to reach a maximum of 350 and 16 units/mg protein, respectively, 8 h after the lesion, remained elevated until 18 h and decreased thereafter to basal values. TNF-alpha levels were maximally elevated (12 units/mg protein) at 3 h and 8 h and returned to basal values by 18 h. Qualitatively similar changes, but with 25-80-fold smaller amplitude, were seen in the contralateral cortex and in the ipsi- and contralateral hippocampus. The levels of IL-6 in the plasma of sham-operated and lesioned rats were only slightly elevated, whereas IL-1 and TNF-alpha were undetectable. Histological studies of brain tissue at early stages after trauma demonstrated an acute hemorrhage associated with neutrophil invasion. The administration of Ro5 4864 (0.5 mg/kg i.p.), a specific ligand of p (peripheral-type benzodiazepine) binding sites, did not result in any significant effect on the levels of IL-6, IL-1 or TNF-alpha in the brain of control or sham-operated animals. However, when administered 24 h before or 15 min after trauma, this benzodiazepine enhanced the increase of these cytokines by 2-4-fold in the ipsilateral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)Journal of Neuroimmunology 03/1993; 42(2):177-85. · 2.47 Impact Factor
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ABSTRACT: Asthma is characterized by difficulty in breathing because of the constriction of the smooth muscles of the bronchi, as a result of inflammation. In the present study, we focus on the protective effects of allantoin against ovalbumin (OVA)-induced lung inflammation in a murine allergic model, and assess cytokine release, eosinophilia, and mucus hypersecretion. Allantoin treatment led to significant reduction in the levels of Ig(immunoglobulin)E and T-helper-2-type cytokines, such as IL(interleukin)-4 and IL-5, in bronchoalveolar lavage (BAL) fluid. Airway inflammatory-cell infiltration was remarkably alleviated in allantoin-treated asthma groups, compared with the control group. Moreover, allantoin-treated asthma groups exhibited a marked decrease in cytokine mRNA expression in lung tissues, compared with the control group. The effectiveness of allantoin was similar to that of montelukast, used as a positive control. These results support the utility of allantoin as a protective agent against asthma.International immunopharmacology 04/2010; 10(4):474-80. DOI:10.1016/j.intimp.2010.01.008 · 2.47 Impact Factor
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