353 resultados para healing gastric ulcer
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The effect of three new derivatives from dehydrocrotonin (DHC-compound I) on gastric damage indifferent animal models including gastric ulceration induced by a necrotic agent and hypothermic restrained-stress was studied: compound 11 (produced by reducing the cyclohexenone moiety of DHC with NaBH4): compound III (produced by reducing the carbonyls with LiAlH4); and compound IV (produced by transforming the lactone moiety into an amide). Their structures were confirmed on the basis of chemical and physicochemical evidence. When previously administered (p.o.) at a dose of 100 mg/kg, compound II significantly (P < 0.01) reduced gastric injury induced by HCl/ethanol (78%) and indomethacin (88%) better than did reference compound 1 (48 and 43%, respectively). But the anti-ulcerogenic activity of compound II was completely abolished by the stress-induced ulcer. Reduction of carbonyls with LiAlH4 (compound 111) caused decreased activity, markedly when no protective effect in any of the models was applied (P > 0.05). However, compound IV, in which the lactone moiety was changed into an amide. when administered at the same dose (100 mg/kg, p.o.), was more effective. The presence of a lactone moiety or Michael acceptor is probably essential for the anti-ulcerogenic effect of these compounds. (C) 2003 Elsevier B.V. Ireland Ltd. All rights reserved.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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The present study reveals the pharmacological action of Serjania erecta Radlk. (Family Sapindaceae), an important medicinal plant species used in the Brazilian Pantanal against gastric pain. The methanolic (Me) and chloroformic (Se) extracts obtained from leaves of S. erecta were challenged by a very strong necrotizing agent in rodents, absolute ethanol. Se was also confronted with a nitric oxide synthase inhibitor (N(G)-nitro-l-arginine methyl ester), a capsaicin cation channel transient receptor potential vanilloid type 1 antagonist (ruthenium red), or a sulfhydryl-blocker (N-ethylmaleimide) to evaluate the participation of these cytoprotective factors in gastroprotection. In an in vivo experimental model, Me and Se presented several degrees of gastroprotective action without signs of acute toxicity. The best gastroprotective effect was restricted to all doses of Se. The mechanisms involving the gastroprotective action of Se are related to an augmented defense mechanism of the gastrointestinal mucosa consisting of sensory neurons, nitric oxide, and sulfhydryl groups that prevent and attenuate the ulcer process. The presence of polyisoprenoids in the Se explains the potent gastroprotective action of this medicinal species. Effective gastroprotective action and the absence of acute toxicity indicate this species may be a promising herbal drug against gastric disease.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Digestion affects acid-base status, because the net transfer of HCl from the blood to the stomach lumen leads to an increase in HCO3- levels in both extra- and intracellular compartments. The increase in plasma [HCO3-], the alkaline tide, is particularly pronounced in amphibians and reptiles, but is not associated with an increased arterial pH, because of a concomitant rise in arterial Pco(2) caused by a relative hypoventilation. In this study, we investigate whether the postprandial increase in Paco(2) of the toad Bufo marinus represents a compensatory response to the increased plasma [HCO3-] or a state-dependent change in the control of pulmonary ventilation. To this end, we successfully prevented the alkaline tide, by inhibiting gastric acid secretion with omeprazole, and compared the response to that of untreated toads determined in our laboratory during the same period. In addition, we used vascular infusions of bicarbonate to mimic the alkaline tide in fasting animals. Omeprazole did not affect blood gases, acid-base and haematological parameters in fasting toads, but abolished the postprandial increase in plasma [HCO3-] and the rise in arterial Pco(2) that normally peaks 48 h into the digestive period. Vascular infusion of HCO3-, that mimicked the postprandial rise in plasma [HCO3-], led to a progressive respiratory compensation of arterial pH through increased arterial Pco(2) Thus, irrespective of whether the metabolic alkalosis is caused by gastric acid secretion in response to a meal or experimental infusion of bicarbonate, arterial pH is being maintained by an increased arterial Pco(2). It seems, therefore, that the elevated Pco(2), occuring during the postprandial period, constitutes of a regulated response to maintain pH rather than a state-dependent change in ventilatory control. (C) 2003 Elsevier B.V. All rights reserved.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)