Effect of a Novel Water-Soluble Vitamin E Derivative, 2-(.ALPHA.-D-Glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol, on Dextran Sulfate Sodium-Induced Colitis in Mice

Naito, Yuji; Takagi, Tomohisa; Matsuyama, Kiichi; Yagi, Nobuaki; Yoshida, Norimasa; Murase, Hironobu; Yoshikawa, Toshikazu

doi:10.3164/jcbn.31.59

Cited by 10 publications

(8 citation statements)

References 38 publications

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“…subsequent disruption of membrane integrity, suggesting that lipid peroxidation mediated by oxygen radicals is an important cause of damage and destruction of cell membranes [35,36]. Our data support another recent finding in our laboratory, in which colonic TBA-reactive substances were markedly reduced by treatment with Mn-superoxide dismutase [37] and a synthetic vitamin E analogue [38] in the same DSS colitis mouse model; this suggests that induction of lipid peroxidation is an early critical event in this experimental inflammatory bowel disease. However, neither PHGG nor SCFA have been reported to have antioxidant activities in vitro, especially the inhibition of lipid peroxidation.…”

Section: Discussionsupporting

confidence: 93%

Partially hydrolyzed guar gum down-regulates colonic inflammatory response in dextran sulfate sodium-induced colitis in mice

Naito

Takagi

Katada

et al. 2006

The Journal of Nutritional Biochemistry

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Section: Discussionsupporting

confidence: 93%

Partially hydrolyzed guar gum down-regulates colonic inflammatory response in dextran sulfate sodium-induced colitis in mice

Naito

Takagi

Katada

et al. 2006

The Journal of Nutritional Biochemistry

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“…Polyunsaturated fatty acids of cell membranes are degraded by lipid peroxidation with subsequent disruption of membrane integrity, suggesting that lipid peroxidation mediated by oxygen radicals is an important cause of damage and destruction of cell membranes (25,26). Our data support another recent finding in our laboratory, in which colonic TBA-reactive substances were markedly reduced by treatment with Mn-superoxide dismutase (27) and a synthetic vitamin E analogue (28) in the same DSS colitis mouse model; this suggests that induction of lipid peroxidation is an early critical event in this experimental inflammatory bowel disease model. However, the present data showed that rosuvastatin did not scavenge hydroxyl or superoxide radicals in vitro.…”

Section: Discussionsupporting

confidence: 82%

Rosuvastatin, a new HMG-CoA reductase inhibitor, reduces the colonic inflammatory response in dextran sulfate sodium-induced colitis in mice

Naito¹,

Katada²,

Takagi³

et al. 2006

Int J Mol Med

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Abstract. The aim of the present study was to elucidate the beneficial effects of rosuvastatin, a new HMG-CoA reductase inhibitor, on colonic mucosal damage and on the inflammatory response in a dextran sulfate sodium (DSS) colitis model. Acute colitis was induced using 8% DSS in female BALB/c mice. Colonic mucosal inflammation was evaluated clinically, biochemically, and histologically. Mucosal protein contents and mRNA levels of tumor necrosis factor (TNF)-· were determined by immunoassay and real time-PCR. The mRNA levels of endothelial nitric oxide synthase (eNOS) were determined by real-time PCR. Disease activity scores in DSSinduced colitis model mice, as determined by weight loss, stool consistency, and blood in stool, were significantly lower in the rosuvastatin-treated mice than in control mice. Shortening of the colon was significantly reversed by rosuvastatin. Increases in tissue-associated myeloperoxidase activity and thiobarbituric acid-reactive substances after DSS administration were both significantly inhibited by treatment with rosuvastatin. Rosuvastatin also inhibited increases in intestinal TNF-· protein and mRNA expression after DSS administration, respectively. The mucosal mRNA levels of eNOS were decreased after DSS administration, but preserved in mice treated with rosuvastatin. These results suggest that rosuvastatin prevents the development of DSS-induced colitis in mice via the inhibition of mucosal inflammatory responses associated with the preservation of eNOS transcription.

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“…We have shown in a model of TNB-induced colitis that thiobarbituric (TBA)-reactive substances, an index of lipid peroxidation, signifi cantly accumulate in the colonic mucosa, 47 and that treatment with SOD leads to an improvement in the colitis score. We have also demonstrated that TBA-reactive substances are signifi cantly increased in the colonic mucosa after DSS administration, and that this increase is signifi cantly inhibited by treatment with MnSOD 35 and a synthetic vitamin E analog 48 in the same DSS colitis mouse model; these results suggest that induction of lipid peroxidation associated with superoxide production is an early critical event in this experimental IBD model.…”

Section: Lipid Peroxidationmentioning

confidence: 82%

Molecular fingerprints of neutrophil-dependent oxidative stress in inflammatory bowel disease

2007

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Neutrophil accumulation within epithelial crypts and in the intestinal mucosa directly correlates with clinical disease activity and epithelial injury in inflammatory bowel disease (IBD). Current advances have defined the mechanisms by which neutrophils are activated or migrate across endothelial and mucosal epithelial cells. A better understanding of this process will likely provide new insights into novel treatment strategies for IBD. Especially, activated neutrophils produce reactive oxygen and nitrogen species and myeloperoxidase within intestinal mucosa, which induce oxidative stress. Posttranslational modification of proteins generated by these reactive species serves as a "molecular fingerprint" of protein modification by lipid peroxidation-, nitric oxide-, and myeloperoxidase-derived oxidants. Measurement of these modified proteins may serve both as a quantitative index of oxidative stress and an important new biological marker of clinical relevance to IBD. We have succeeded in the clinical development of a novel granulocyte adsorptive apheresis therapy for IBD. In this review, we discuss current advances in defining the role of neutrophil-dependent oxidative stress in IBD.

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Effect of a Novel Water-Soluble Vitamin E Derivative, 2-(.ALPHA.-D-Glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol, on Dextran Sulfate Sodium-Induced Colitis in Mice

Cited by 10 publications

References 38 publications

Partially hydrolyzed guar gum down-regulates colonic inflammatory response in dextran sulfate sodium-induced colitis in mice

Partially hydrolyzed guar gum down-regulates colonic inflammatory response in dextran sulfate sodium-induced colitis in mice

Rosuvastatin, a new HMG-CoA reductase inhibitor, reduces the colonic inflammatory response in dextran sulfate sodium-induced colitis in mice

Molecular fingerprints of neutrophil-dependent oxidative stress in inflammatory bowel disease

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