Inhibitory effect of DS-4574, a peptidoleukotriene antagonist with mast cell stabilizing action, on compound 48/80-induced gastric mucosal lesions in rats

Tabuchi, Yoshiaki; Kawarabayashi, Keiko; Furuhama, Kazuhisa

doi:10.1007/bf01986388

Cited by 4 publications

(4 citation statements)

References 22 publications

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“…A number of articles have reported that several histamine H1-receptor antagonists (eg, olopatadine, desloratadine, pyrilamine maleate, and ketotifen) [87][88][89] and inhibitors of peptidoleukotriene 90 can stabilize mast cells and decrease their mediator release. It appears that histamine and peptidoleukotriene released from mast cells can render mast cells more active in releasing mediators, suggesting that the pool of mast cells has a positive-feedback, selfenhancing amplification mechanism of mediator release.…”

Section: Pharmacologic Mediators Of Mast Cellsmentioning

confidence: 98%

Anti-IgE as a mast cell–stabilizing therapeutic agent

Chang

Shiung

2006

Journal of Allergy and Clinical Immunology

116

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Section: Pharmacologic Mediators Of Mast Cellsmentioning

confidence: 98%

Anti-IgE as a mast cell–stabilizing therapeutic agent

Chang

Shiung

2006

Journal of Allergy and Clinical Immunology

116

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“…Administration of SCG has been shown to block hypersecretory response to both histamine and gastrin in iodacetamide-induced gastritis in mice (Piqueras et al, 2003). SCG also inhibits gastric acid secretion in response to ulcerogens, pentagastrin and C48/80 in rats (Tabuchi et al, 1994;Nicol et al, 1981).…”

Section: Discussionmentioning

confidence: 97%

“…Recently, mast cells have been implicated in the pathogenesis of Helicobacter pylori-infected gastritis (Nakajima et al, 2004) whereas stabilization of mast cells has been suggested to be a key mechanism to protect the gastrointestinal tract from injury (Penissi et al, 2003). Involvement of mast cells in gastropathy is supported by the fi ndings of animal studies showing the induction of gastric mucosal lesions by mast cell degranulators (Ohta et al, 2003;Kawakubo et al, 2005;Tabuchi et al, 1994) and their protection by mast cell stabilizers (Tabuchi et al, 1994;Ali, 1995;Erkasap et al, 2005;Takeuchi et al, 1986).…”

Section: Introductionmentioning

confidence: 89%

Protective effects of nedocromil sodium and sodium cromoglycate on gastroduodenal ulcers: a comparative study in rats

et al. 2006

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Stabilization of mast cells plays a key mechanism to protect gastrointestinal tract from injury. This study presents a comparative evaluation of mast cell stabilizers nedocromil sodium (NDS) and sodium cromoglycate (SCG) in experimental gastric and duodenal ulcers in rats. Wistar rats of either sex were used in this study. Both NDS and SCG, in the doses of 10, 30 and 100 mg/kg were given intraperitoneally for gastric secretion studies and by gavage for antiulcer studies. Acid secretion studies were undertaken in pylorus-ligated rats. Gastric lesions were induced by water immersion restraint stress (WIRS), indomethacin and ethanol whereas duodenal ulcers were produced by cysteamine. The level of glutathione (GSH) and gastric wall mucus were measured in glandular stomach of rats following ethanol-induced gastric lesions. SCG was more effective than NDS in preventing WIRS- and indomethacin-induced gastric lesions whereas reverse was true in ethanol- and cysteamine-induced ulcers. All the 3 doses of SCG offered almost equal protection against WIRS-induced gastric lesions whereas only medium and high dose of NDS provided significant protection in this model of ulcer. NDS significantly inhibited cysteamine-induced duodenal ulcers whereas SCG failed to do so. Pretreatment with NDS or SCG significantly and dose-dependently protected gastric mucosa against ethanol-induced injury, while the former drug appeared to be more effective. The cytoprotective effects of these two drugs were accompanied by the attenuation of ethanol-induced depletion of gastric wall mucus and GSH. The differential effects of NDS and SCG against various gastric lesions rationalize the possible benefits of a combined therapy (NDS+SCG) for the treatment of complex gastroduodenal ulcers.

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“…LY171883 was chosen as an inhibitor of the LTD 4 receptor (Fig. 1) with the dose selected based on the work of Tabuchi et al (1994).…”

Section: Introductionmentioning

confidence: 99%

Role of leukotrienes in N-(3,5-dichlorophenyl)succinimide (NDPS) and NDPS metabolite nephrotoxicity in male Fischer 344 rats

Rankin¹,

Hong²,

Anestis³

et al. 2012

Toxicology

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The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) can induce marked nephrotoxicity in rats following a single intraperitoneal (ip) administration of 0.4 mmol/kg or greater. Although NDPS induces direct renal proximal tubular toxicity, a role for renal vascular effects may also be present. The purpose of this study was to examine the possible role of vasoconstrictor leukotrienes in NDPS and NDPS metabolite nephrotoxicity. Male Fischer 344 rats (4 rats/group) were administered diethylcarbamazine (DEC; 250 or 500 mg/kg, ip), an inhibitor of LTA4 synthesis, 1h before NDPS (0.4 mmol/kg, ip), N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS, 0.1, 0.2, or 0.4 mmol/kg, ip), or N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA, 0.1 mmol/kg, ip) or vehicle. In a separate set of experiments, the LTD4 receptor antagonist LY171883 (100 mg/kg, po) was administered 0.5 h before and again 6 h after NDHS (0.1 mmol/kg, ip) or 2-NDHSA (0.1 mmol/kg, ip) or vehicle. Renal function was monitored for 48 h post-NDPS or NDPS metabolite. DEC markedly reduced the nephrotoxicity induced by NDPS and its metabolites, while LY171883 treatments provided only partial attenuation of NDHS and 2-NDHSA nephrotoxicity. These results suggest that leukotrienes contribute to the mechanisms of NDPS nephrotoxicity.

show abstract

Inhibitory effect of DS-4574, a peptidoleukotriene antagonist with mast cell stabilizing action, on compound 48/80-induced gastric mucosal lesions in rats

Cited by 4 publications

References 22 publications

Anti-IgE as a mast cell–stabilizing therapeutic agent

Anti-IgE as a mast cell–stabilizing therapeutic agent

Protective effects of nedocromil sodium and sodium cromoglycate on gastroduodenal ulcers: a comparative study in rats

Role of leukotrienes in N-(3,5-dichlorophenyl)succinimide (NDPS) and NDPS metabolite nephrotoxicity in male Fischer 344 rats

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