Yasunari Sugawa's research while affiliated with Kyoto Pharmaceutical University and other places
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Publications (10)
To investigate the EP receptor subtype involved in the gastroprotective action of prostaglandin (PG) E2 using various EP receptor agonists in rats, and using knockout mice lacking EP1 or EP3 receptors.
Male SD rats and C57BL/6 mice were used after an 18-h fast. Gastric lesions were induced by oral administration of HCl/ethanol (150 mM HCl in 60% et...
We investigated the role of luminal Ca2+ in the regulation of nitric oxide (NO) release and acid secretion in the rat stomach following damage by sodium taurocholate (TC). Under urethane anesthesia, a rat stomach was mounted in an ex vivo chamber, perfused with saline, and transmucosal potential difference (PD), luminal pH, acid secretion, and lumi...
The effects of a nitric oxide (NO)-releasing derivative of aspirin, NCX-4016, on gastric functional and ulcerogenic responses in rat stomachs were examined in comparison with those of aspirin. Topical application of aspirin (80 mM) to the stomach markedly decreased transmucosal potential difference and slightly increased luminal pH (acid back-diffu...
We examined the effect of NO synthase inhibitor on the functional and ulcerogenic responses to aspirin (ASA) in rat stomach. The animals were given ASA (20-80 mM) orally with or without HCl (10-50 mM) and killed 2 h later. NG-nitro-L-arginine methyl ester (L-NAME) was given i.v. 5 min before aspirin. In the functional study, a rat stomach was mount...
Inhibitory effect of galanin on basal and secretagogs-stimulated gastric acid secretion was investigated in urethane-anesthetized rats. A rat stomach was mounted in an ex-vivo chamber, perfused with saline, and either gastric acid or alkaline secretion was determined by titrating the perfusate. Gastric mucosal blood flow (GMBF) was measured by a la...
We previously reported the impaired HCO3- secretion and the increased mucosal susceptibility to acid in the duodenum of streptozotocin (STZ)-induced diabetic rats. In this study, we investigated the salutary effect of the NO synthase inhibitor L-NAME (NG-nitro-L-arginine methyl ester) on these changes and compared it with those of insulin. Animals...
Citations
... L-NAME prevents the later extension of b cell destruction, resulting in the antidiabetogenic effect. Alternatively, it might be possible that NO exerts a negative influence on glucose transport and that L-NAME stimulates cellular uptake of glucose by antagonizing such NO effect [18]. When compared with diabetic group, in our study the decrease in blood glucose levels at STZ + L-NAME group was not significant. ...
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... 63 The absence of toxic GI effects of NO-NSAIDs, such as NCX-4016 (NO-aspirin) and NCX-530 (NO-indomethacin) against HCl/ethanol-induced damage. 35,59,64 Is also confirmed NCX-4016 (NO-aspirin) GI safety in either normal or diabetic rat stomachs. 65 The strong evidence of the therapeutic potential of NSAIDs in several clinical scenarios, together with their gastric safety, has made it possible to explore their use at higher doses and in conjunction with other medications, if necessary. ...
... Moreover, according to numerous studies, GAL is involved in the control of food intake [43][44][45] and appetite [43,46]. Furthermore, inhibitory effects of GAL on gastric acid secretion was reported in rats [47,48], and is a convergent result to that observed under the influence of CART, as described above. Previous studies also showed that GAL can modulate gastric motility in rats, depending upon the receptor subtype activation [49]. ...
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... As a result, the decision to initiate or cease LDA intake must be cautiously weighed, as discontinuation may lead to a twofold increase in cardiovascular event risk [8][9][10]. The impact of aspirin on the GI mucosa arises from its irreversible inhibition of the cyclooxygenase enzyme (COX) essential for prostaglandin synthesis [11][12][13]. This mechanism also contributes to PU development [13,14]. ...
... Some of such mechanisms have been shown to cause Ca 2+ mobilization that is highly localized, brief increases in Ca 2+ while other pathway mechanisms produce longer-lasting elevations of Ca 2+ , which often follow oscillations caused by feedback loops within the signaling system (Berridge, 1997). In vivo gastric damage elicits increased gastric luminal Ca 2+ (Koo, 1994;Takeuchi, Kato, Konaka, & Sugawa, 1999;Takeuchi et al., 1985). While intracellular Ca 2+ appears to be localized within the cells adjacent to the damaged site, previous studies have been limited in investigating Ca 2+ mobilization within an in vitro model that closely mirrors in vivo native, noncancerous tissue. ...
... El efecto antiinflamatorio y regenerador celular del consumo de perejil se relaciona a la presencia de polifenoles y aceites esenciales que estarían ligados a la regulación de la síntesis de prostaglandinas en el tejido gástrico, una de cuyas funciones es la protección de la mucosa gástrica (11) . El etanol, en ratas, ocasiona daño en el tejido gástrico; ante ello, las células protegen la integridad del epitelio mediante la angiogénesis. ...
