Aminoguanidine prevents concanavalin A-induced hepatitis in mice

Okamoto, Toshihiro; Masuda, Yasuhisa; Kawasaki, Toru; Shinohara, Motoki; Matsuzaki, K.

doi:10.1016/s0014-2999(00)00186-2

Cited by 19 publications

(10 citation statements)

References 15 publications

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“…There are three isoforms of NOx synthase; eNOS which is found in the endothelial cells, nNOS which is found in neurons and iNOS which is induced by cytokines such as TNF‐α . Previous investigations have shown that Con A injection causes upregulation of iNOS mRNA expression and the released NO is suggested to exacerbate Con A‐induced hepatitis . These reports are in accordance with the results of this study as Con A induced a significant elevation of NOx level, which was counteracted by PFD pretreatment.…”

Section: Discussionsupporting

confidence: 92%

Pirfenidone ameliorates concanavalin A-induced hepatitis in mice via modulation of reactive oxygen species/nuclear factor kappa B signalling pathways

El‐Agamy

2016

Journal of Pharmacy and Pharmacology

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Section: Discussionsupporting

confidence: 92%

Pirfenidone ameliorates concanavalin A-induced hepatitis in mice via modulation of reactive oxygen species/nuclear factor kappa B signalling pathways

El‐Agamy

2016

Journal of Pharmacy and Pharmacology

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“…However, high induction of iNOS with subsequent overproduction of NO involves complex responses in tissues which has led to some debate regarding the effect of iNOS on carcinogenesis. For example, some studies have reported protection after inhibition of iNOS [13][14][15] while others have reported exacerbation of the carcinogenic process. 16 17 Advances in recombinant DNA technology have permitted the development of mice that specifically lack the capacity to express the iNOS gene.…”

mentioning

confidence: 99%

Decreased Helicobacter pylori associated gastric carcinogenesis in mice lacking inducible nitric oxide synthase

Nam

et al. 2004

Gut

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Background and aims: Overproduction of nitric oxide via inducible nitric oxide synthase (iNOS) is suggested to be a significant pathogenic factor in Helicobacter pylori induced gastritis. The purpose of this study was to examine the role of iNOS in H pylori associated gastric carcinogenesis. Methods: Two types of mice were used in this study: iNOS deficient mice (iNOS2/2) and wild-type littermates. Gastric cancer was generated in mice using a combination treatment comprising N-methyl-Nnitrosourea administration and H pylori infection. Fifty weeks after treatment, tumours in gastric tissues from both types of mice were examined using histopathology, immunohistochemistry, and immunoblotting for iNOS and 3-nitrotyrosine. Results: The overall incidence of gastric cancer at week 50 was significantly lower in iNOS2/2 compared with iNOS wild-type mice (p,0.05). When analysed according to tumour pathology, the incidence of gastric adenocarcinoma was significantly lower in iNOS2/2 compared with iNOS wild-type mice (p,0.05). Immunostaining for iNOS was clearly observed in adenocarcinoma cells of iNOS wild-type mice, and was characterised by a strong cytoplasmic expression pattern. 3-Nitrotyrosine was expressed mostly in the area of the lamina propria of gastritis and adenoma lesions in iNOS wild-type mice. Immunoblotting analyses showed that iNOS and 3-nitrotyrosine were also expressed in both adenoma and adenocarcinoma tissues from iNOS wild-type mice. iNOS and 3-nitrotyrosine expression was greater in tumour tissues than in non-tumour tissues. Conclusions: These findings suggest that iNOS contributes to H pylori associated gastric carcinogenesis in mice.

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“…1A. Since elevation of plasma ALT and morpho-logical changes in the liver are correlated (11,12), the effect of coumarins on hepatitis was evaluated by measuring plasma ALT. Mice were pretreated with 200 mg/ kg (i.p.)…”

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confidence: 99%

Inhibition of Concanavalin A-Induced Mice Hepatitis by Coumarin Derivatives

Yoshida

Kobayashi

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-The effects of coumarin derivatives, osthole, imperatorin, Pd-Ia, Pd-II and Pd-III, on mice concanavalin A (Con A) (0.2 mg/mouse, i.v.)-induced hepatitis were studied. At the dose of 200 mg/ kg (i.p.), these coumarins inhibited more than 90% of the Con A-induced elevation of plasma alanine aminotransferase activity, but glycyrrhizin (200 mg / kg, i.p.) caused only 45% inhibition. At the dose of 100 mg/ kg (i.p.), osthole produced the strongest inhibition among these coumarins. The inhibitory activity of osthole is lost when its 7-methoxy group is replaced by a 7-hydroxy group to form osthenol. The present results showed that coumarin derivatives inhibited Con A-induced hepatitis, with osthole being the most inhibitory.

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Aminoguanidine prevents concanavalin A-induced hepatitis in mice

Cited by 19 publications

References 15 publications

Pirfenidone ameliorates concanavalin A-induced hepatitis in mice via modulation of reactive oxygen species/nuclear factor kappa B signalling pathways

Pirfenidone ameliorates concanavalin A-induced hepatitis in mice via modulation of reactive oxygen species/nuclear factor kappa B signalling pathways

Decreased Helicobacter pylori associated gastric carcinogenesis in mice lacking inducible nitric oxide synthase

Inhibition of Concanavalin A-Induced Mice Hepatitis by Coumarin Derivatives

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