Irsogladine maleate suppresses indomethacin-induced elevation of proinflammatory cytokines and gastric injury in rats

Zhang, Xin; Tajima, Koyuki; Kageyama, Kiyoto; Kyoi, Takashi

doi:10.3748/wjg.14.4784

Cited by 39 publications

(23 citation statements)

References 27 publications

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“…The experimental model depends upon consumption of kefir with suitable properties. In Table 2, the analysis results of the kefir, which were only for 1-2 days, were in agreement with the findings of other researchers regarding the general composition and microbiologic appearance of kefir; especially from the perspective of probiotic effect, Lactobacillus and Streptococcus genus showed that they were of sufficient degree considering the number (5,(25)(26)(27). The gross composition of raw milk used in the production of kefir was close to the average milk composition (1,3,7,17,26,27).…”

Section: Discussionsupporting

confidence: 79%

A study on the protective activity of kefir against gastric ulcer

Orhan

Karagözlü

Sarıoğlu³

et al. 2012

Turk J Gastroenterol

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Section: Discussionsupporting

confidence: 79%

A study on the protective activity of kefir against gastric ulcer

Orhan

Karagözlü

Sarıoğlu³

et al. 2012

Turk J Gastroenterol

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“…Activated neutrophils are a potential source of oxygen metabolites which initiate the deactivation of antiproteases and activating cytotoxic enzymes including elastase, proteases, lactoferrin and MPO. 32,33) Result revealed that the tacrolimus treated group had decreased MPO activity, so this may be due to the drug's immunosuppressive action.…”

Section: Discussionmentioning

confidence: 99%

Activity of Tacrolimus: An Immunosuppressant, in Pyloric Ligation Induced Peptic Ulcer in Rat

Sood

Muthuraman

2009

YAKUGAKU ZASSHI

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The eŠect of tacrolimus (FK506) on peptic ulcer was evaluated using pyloric ligation (PL) model in rats. Tacrolimus was administered orally at diŠerent doses (1, 2 and 3 mg/kg) and it showed a gastric ulcer healing eŠect in a dose dependent manner. Gastric volume, total and free acidity and ulcerative index parameters were reduced in the tacrolimus treated rats as compared to pyloric ligated rats. The higher dose (3 mg/kg) treated group produced signiˆcant results similar to that of the ranitidine (50 mg/kg) treated group. Pretreatment with tacrolimus also produced signiˆcant (p＜ 0.05) reduction in TBARS, total calcium, TNF-a, IL-8 and MPO whereas it showed an increase in GSH level at higher dose. The anti-secretory and anti-ulcerative eŠect of tacrolimus may be due to immunosuppressive actions by inhibition of calcineurin and the oxidative pathway. It can be concluded that tacrolimus can play an important role in the treatment of peptic ulcer disorder to improve the quality of life.

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“…A PPI was administered 30 min before indomethacin administration: omeprazole (30, 100 mg/kg), lansoprazole (30, 100 mg/kg), or rabeprazole (30, 100 mg/kg). The following were administered twice-30 min before and 6 h after indomethacin administration: an H 2 receptor antagonist (famotidine (3, 10 mg/kg), cimetidine (100 mg/kg), lafutidine [50] (30 mg/kg), or roxatidine [51] (60, 100, 200 mg/kg)); a mucosal protective agent (teprenone [52] (100, 300 mg/kg), rebamipide [53] (100, 300 mg/kg), irsogladine [54] (1, 10 mg/kg), ecabet sodium [55] (300 mg/kg)); sucralfate (500 mg/kg) or a PG analog (misoprostol (0.1 mg/kg)).…”

Section: Prevention and Treatment Of Small Intestinal Mucosal Injury mentioning

confidence: 99%

Present status and strategy of NSAIDs-induced small bowel injury

et al. 2009

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Non-steroidal anti-inflammatory drugs (NSAIDs) are well known to cause gastroduodenal mucosal lesions as an adverse effect. Recently, the serious problem of NSAID-induced small intestinal damage has become a topic of great interest to gastroenterologists, since capsule endoscopy and balloon enteroscopy are available for the detection of small intestinal lesions. Such lesions have been of great concern in clinical settings, and their treatment and prevention must be devised as soon as possible. The prevalence of NSAIDs-induced small intestinal injury is higher than had been expected. Recent studies show that more than 50% of patients taking NSAIDs have some mucosal damage in the small intestine. The gross appearance of NSAIDinduced enteropathy varies, appearing variously as diaphragm-like strictures, ulcers, erosions, and mucosal redness. To investigate NSAID-induced enteropathy, and to rule out other specific enteropathies, other useful methods (in addition to capsule endoscopy and balloon enteroscopy) include such modalities as radiological examination of the small intestine, the permeability test, scintigraphy or the fecal excretion test using 111 Indium-labeled white blood cells, and measurement of the fecal calprotectin concentration. Diaphragm-like strictures and bleeding from mucosal breaks may be treatable with interventional enteroscopy. Misoprostol, metronidazole, and sulfasalazine are frequently used to treat NSAID-induced enteropathy, but have undesirable effects in some cases. In the experimental model, we confirmed that several existing drugs for gastroduodenal ulcers prevented indomethacin-induced small intestinal injury. Such drugs may be useful for preventing the adverse effects of NSAIDs not only in the stomach but also in the small intestine. We hope to examine these drugs in future clinical studies.

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Irsogladine maleate suppresses indomethacin-induced elevation of proinflammatory cytokines and gastric injury in rats

Abstract: The mucosal protective effects afforded by irsogladine maleate on gastric injury induced by indomethacin are mediated by inhibition of mucosal proinflammatory cytokine production and neutrophil infiltration, leading to suppression of mucosal inflammation and subsequent tissue destruction.

Cited by 39 publications

References 27 publications

A study on the protective activity of kefir against gastric ulcer

A study on the protective activity of kefir against gastric ulcer

Activity of Tacrolimus: An Immunosuppressant, in Pyloric Ligation Induced Peptic Ulcer in Rat

Present status and strategy of NSAIDs-induced small bowel injury

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