Sodium alginate ameliorates indomethacin-induced gastrointestinal mucosal injury<i>via</i>inhibiting translocation in rats

Yamamoto, Atsuki; Itoh, Tomokazu; Nasu, Reishi; Nishida, Ryuichi

doi:10.3748/wjg.v20.i10.2641

Cited by 31 publications

(31 citation statements)

References 34 publications

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“…Dengiz, Odabasoglu, Halici, Cadirci, and Suleyman () found increased CAT activity in indomethacin‐induced gastric ulcer. Yamamoto, Itoh, Nasu, and Nishida () found decreased GPx activity as parallel to our study, but reported diminished CAT and SOD activities in indomethacin‐induced small intestinal injury. An elevated activity of CAT and SOD were observed in this study.…”

Section: Discussionsupporting

confidence: 89%

“…Dengiz, Odabasoglu, Halici, Cadirci, and Suleyman (2007) found increased CAT activity in indomethacin-induced gastric ulcer. Yamamoto, Itoh, Nasu, and Nishida (2014) of protein damage. Vit C, Vit E, β-carotene, Se combination, and also ranitidine were found to attenuate indomethacin-induced effects, probably due to halting of the deleterious effect of free radicals (Table 3).…”

Section: Discussionmentioning

confidence: 99%

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The effects of vitamins and selenium mixture or ranitidine against small intestinal injury induced by indomethacin in adult rats

et al. 2019

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This study was aimed at investigating morphological and biochemical efficacies of antioxidants on indomethacin‐induced small intestinal damage in rats. Group I: control animals (negative control) given only placebo, Group II: (positive control) are animals orally given combination of antioxidants [vitamin C (Vit C), vitamin E (Vit E), β‐carotene and sodium selenite (Se)] daily for 3 days, Group III: Rats were given only indomethacin, Group IV: animals were given of antioxidants combination for 3 days, last dose was given 2 hr before the administration of indomethacin. Group V: Animals receiving ranitidine for 3 days (second positive control). Group VI: Animals received ranitidine for 3 days, last dose was given 2 hr before to indomethacin administration. Indomethacin caused degenerative morphological and biochemical changes, which were reversed on antioxidants administration. As a result, we propose that antioxidants combination would be therapeutically beneficial for treating indomethacin‐induced lesions of small intestine. Practical applications Indomethacin is a widely preferred nonsteroidal anti‐inflammatory drug (NSAID) but its side effects on gastrointestinal system are well known. Indomethacin also causes production of reactive oxygen species. Antioxidants and selenium has protective effects. According to the results of this study, antioxidants and selenium can be used as a food supplement for preventing NSAID‐induced side effects and toxicity.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

The effects of vitamins and selenium mixture or ranitidine against small intestinal injury induced by indomethacin in adult rats

et al. 2019

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“…The majority of experimental studies on NSAID-enteropathy have used single, highdose indomethacin administration to induce mucosal damage. In these models, the injury pattern consists mainly of multiple, hemorrhagic lesions involving the full thickness of intestinal wall [48,49,50], a picture that differ greatly from the ones seen at enteroscopy or video capsule endoscopy in patients taking NSAIDs chronically [11,12,13]. Most importantly, these acute models of intestinal damage may be not suitable to evaluate the protective effect of poorly absorbed antibiotics, like rifaximin, which need at least 7-10 days to consistently affect intestinal bacterial load, composition and activity [51].…”

Section: Discussionmentioning

confidence: 99%

“…In a subgroup of animals, treatment with rifaximin was initiated 7 days before starting indomethacin administration and continued for 14 days until the end of treatment with the NSAID. The dose of 50 mg/kg BID had been found to protect against enteropathy induced by indomethacin in a preliminary dose-response study (25,50 and 100 mg/kg BID). In addition, the selected rifaximin dose was similar to that employed in previous studies in rats [38,39].…”

Section: Experimental Designmentioning

confidence: 99%

Small bowel protection against NSAID-injury in rats: Effect of rifaximin, a poorly absorbed, GI targeted, antibiotic

Fornai

Antonioli

Pellegrini

et al. 2016

Pharmacological Research

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Nonsteroidal anti-inflammatory drugs, besides exerting detrimental effects on the upper digestive tract, can also damage the small and large intestine. Although the underlying mechanisms remain unclear, there is evidence that enteric bacteria play a pivotal role. The present study examined the enteroprotective effects of a delayed-release formulation of rifaximin-EIR (R-EIR, 50mg/kg BID, i.g.), a poorly absorbed antibiotic with a broad spectrum of antibacterial activity, in a rat model of enteropathy induced by indomethacin (IND, 1.5mg/kg BID for 14 days) administration. R-EIR was administered starting 7 days before or in concomitance with IND administration. At the end of treatments, blood samples were collected to evaluate hemoglobin (Hb) concentration (as an index of digestive bleeding). Small intestine was processed for: (1) histological assessment of intestinal damage (percentage length of lesions over the total length examined); (2) assay of tissue myeloperoxidase (MPO) and TNF levels, as markers of inflammation; (3) assay of tissue malondialdehyde (MDA) and protein carbonyl concentrations, as an index of lipid and protein peroxidation, respectively; (4) evaluation of the major bacterial phyla. IND significantly decreased Hb levels, this effect being significantly blunted by R-EIR. IND also induced the occurrence of lesions in the jejunum and ileum. In both intestinal regions, R-EIR significantly reduced the percentage of lesions, as compared with rats receiving IND alone. Either the markers of inflammation and tissue peroxidation were significantly increased in jejunum and ileum from IND-treated rats. However, in rats treated with R-EIR, these parameters were not significantly different from those observed in controls. R-EIR was also able to counterbalance the increase in Proteobacteria and Firmicutes abundance induced by INDO. To summarize, R-EIR treatment significantly prevents IND-induced intestinal damage, this enteroprotective effect being associated with a decrease in tissue inflammation, oxidative stress and digestive bleeding as well as reversal of NSAID-induced alterations in bacterial population.

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“…For example, nonsteroidal anti-inflammatory drugs (NSAIDs) are known to damage both gastric and intestinal mucosa. MUC2 expression in intestinal mucosa has been reported to be reduced by mucosal damage caused by NSAIDs [21]. Additionally, intestinal mucosal damage by NSAIDs reduces the number of intestinal microvilli, disrupts the epithelial surface, and opens tight junctions, leading to increased intestinal permeability [22].…”

Section: Toxicological Evaluationsmentioning

confidence: 99%

Intestinal cells differentiated from human induced pluripotent stem cells for use in drug development studies

Iwao

Matsunaga

2019

Translational and Regulatory Sciences

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In drug development studies, various in vitro model systems (such as Caco-2 cells and intestinal microsomes) are widely used for evaluating intestinal pharmacokinetics and toxicological properties of drugs, including the rate of drug absorption, drug metabolism, and extent of mucosal damage. However, these approaches have limited accuracy in predicting intestinal availability and toxicity. To overcome these problems, new approaches have been recently developed to generate intestinal epithelial cells and organoids that are derived from induced pluripotent stem (iPS) cells, which have shown great potential for use in drug development studies. In this review, we summarized our research regarding intestinal epithelial cells and organoids generated from human iPS cells. We demonstrated that intestinal epithelial cells derived from human iPS cells exhibit drug-metabolizing enzyme activities, drug transporter activities, and cytochrome P450 inducibility. We speculated that drug-induced intestinal mucosal damage in derived epithelial cells can be evaluated. Moreover, intestinal organoids derived from human iPS cells were found to contain various intestinal cell types and develop apical-basal polarity. The differentiated organoids have intestine-like structures with desired pharmacokinetic attributes and barrier functions. Intestinal epithelial cells and organoid tissues derived from human iPS cells show great potential to be more widely used in drug development studies, including pharmacokinetic studies, toxicological evaluations, drug screening, and studies on intestinal bowel disease models.

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Sodium alginate ameliorates indomethacin-induced gastrointestinal mucosal injuryviainhibiting translocation in rats

Abstract: These results indicate that AL-Na ameliorates non-steroidal anti-inflammatory drug-induced small intestinal enteritis via bacterial translocation.

Cited by 31 publications

References 34 publications

The effects of vitamins and selenium mixture or ranitidine against small intestinal injury induced by indomethacin in adult rats

The effects of vitamins and selenium mixture or ranitidine against small intestinal injury induced by indomethacin in adult rats

Small bowel protection against NSAID-injury in rats: Effect of rifaximin, a poorly absorbed, GI targeted, antibiotic

Intestinal cells differentiated from human induced pluripotent stem cells for use in drug development studies

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